Vitamin D status in India-Its implications and Remedial Measures

Department of Endocrinology and Metabolism, Sri Venkateswara Institute of Medical Sciences, Tirupati - 517 507, Andhra Pradesh, India.
The Journal of the Association of Physicians of India 01/2009; 57:40-8.
Source: PubMed


Vitamin D deficiency is epidemic in India despite of plenty of sunshine. The interpretation of vitamin D levels should be done with the solar zenith angle, minimal erythemal dose, skintype, UV Index and geographical location. All Indian studies uniformly point to low 25(OH)D levels in the populations studies despite abundant sunshine. All studies have uniformly documented low dietary calcium intake compared to Recommended Daily/Dietary Allowances (RDA) by Indian Council of Medical Research (ICMR). The vitamin D status of children is very low in both urban and rural population studied. Pregnant women and their new born had low vitamin D status. The effect of short course of loading doses of vitamin D doesn't have a lasting effect and a maintenance dose is needed. Low 25(OH)D levels has its implications of lower peak bone mass and lower BMD compared to west. There may be a public health need to fortify Indian foods with vitamin D.

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Article: Vitamin D status in India-Its implications and Remedial Measures

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    • "However, there are no studies in this regard in the southern Indian population with regards to epilepsy. This is relevant in an Indian context, since a high prevalence of vitamin D deficiency has been reported widely in the normal and diseased population.[141516] "
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    ABSTRACT: Background:Although there are reports describing the association of alternations of bone and mineral metabolism in epileptic patients with long-term anticonvulsant therapy, there are only limited Indian studies which have looked at this aspect.Objectives:This study was done to compare the prevalence of changes in bone mineral parameters and bone mineral density (BMD) in ambulant individuals on long-term anticonvulsant therapy with age- and body mass index (BMI)-matched healthy controls.Materials and Methods:There were 55 men (on medications for more than 6 months) and age- and BMI-matched 53 controls. Drug history, dietary calcium intake (DCI), and duration of sunlight exposure were recorded. Bone mineral parameters and BMD were measured.Results:The control group had a significantly higher daily DCI with mean ± SD of 396 ± 91 mg versus 326 ± 101 mg (P = 0.007) and more sunlight exposure of 234 ± 81 vs 167 ± 69 min (P = 0.05). BMD at the femoral neck was significantly lower in cases (0.783 ± 0.105 g/cm2) when compared to controls (0.819 ± 0.114 g/cm2). Majority of the patients (61%) had low femoral neck BMD (P = 0.04). There was no significant difference in the proportion of subjects with vitamin D deficiency (<20 ng/mL) between cases (n = 32) and controls (n = 37) (P = 0.234).Conclusions:Vitamin D deficiency was seen in both the groups in equal proportions, highlighting the existence of a high prevalence of this problem in India. Low femoral neck BMD found in cases may stress the need for supplementing calcium and treating vitamin D deficiency in this specific group. However, the benefit of such intervention has to be studied in a larger proportion of epileptic patients.
    Annals of Indian Academy of Neurology 08/2014; 17(3):272. DOI:10.4103/0972-2327.138489 · 0.60 Impact Factor
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    • "Vitamin D deficiency is a common disorder, found in all age groups and in both genders [1, 2]. It is prevalent in various parts of the world including India [1–3] with an increased occurrence in high and low latitude countries [4]. Worldwide, the prevalence of vitamin D deficiency is 50% in elderly [5] and within Europe in 2%–30% of adults [6]. "
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    ABSTRACT: Background. Vitamin D deficiency is widespread throughout the world. Several reports have incriminated vitamin D deficiency as the cause of rickets, osteomalacia, and other chronic diseases. Recent studies have suggested a possible link between deficiency of 25-hydroxyvitamin D and dyslipidemia. Aim. To investigate the association between 25-hydroxyvitamin D deficiency and dyslipidemia in Indian subjects. Methodology. We recruited 150 asymptomatic consecutive subjects from patients' attendees at the Departments of Neurology and Medicine in Yashoda Hospital, Hyderabad, India. Study period was from October 2011 to March 2012. All subjects underwent 25-hydroxyvitamin D assay by chemiluminescent microparticle immunoassay, fasting blood sugar and lipid profile, calcium, phosphorus, alkaline phosphatase, and C-reactive protein (CRP). Results. Out of 150 subjects, men were 82 (54.6%), and mean age was 49.4 (±15.6) years. Among risk factors, hypertension was noted in 63/150 (42%), 25-hydroxyvitamin D deficiency in 59/150 (39.3%), diabetes in 45/150 (30%), dyslipidemia in 60 (40%), smoking in 35/150 (23.3%), and alcoholism in 27/150 (18%). Deficiency of 25-hydroxyvitamin D was significantly associated with dyslipidemia (P = 0.0001), mean serum glucose (P = 0.0002) mean CRP (P = 0.04), and mean alkaline phosphatase (P = 0.01). Multivariate analysis showed that 25-hydroxyvitamin D deficiency was independently associated with dyslipidemia (odds ratio: 1.9; 95% CI : 1.1-3.5). Conclusions. We found that deficiency of 25-hydroxyvitamin D was independently associated with dyslipidemia in Indian subjects.
    12/2013; 2013(3):623420. DOI:10.1155/2013/623420
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    • "Vitamin D deficiency (VDD) has been documented across all age groups and both sexes from India and different parts of world [1] [2]. According to a recent studies conducted in Indian population VDD was noted in more than 90% population [2] [3] [4] [5]. VDD is defined as serum 25-hydroxy vitamin D (25OHD) levels <20 ng/ml [6]. "
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    ABSTRACT: The main physiological function of vitamin D is maintenance of calcium homeostasis by its effect on calcium absorption, and bone health in association with parathyroid gland. Vitamin D deficiency (VDD) is defined as serum 25-hydroxy vitamin D (25OHD) levels <20ng/ml. Vitamin D insufficiency is called when serum 25OHD levels are between 20-29ng/ml, though existence of this entity has been questioned. Do all subjects with VDD have clinical disease according to this definition? Analysis of published studies suggests that calcium absorption in inversely correlated with serum 25OHD levels and calcium intake. We hypothesize that there exist an intestinal calcistat, which controls the calcium absorption independent of PTH levels. It consists of calcium sensing receptor (CaSR) on intestinal brush border, which senses calcium in intestinal cells and vitamin D system in intestinal cells. CaSR dampens the generation of active vitamin D metabolite in intestinal cells and decrease active transcellular calcium transport. It also facilitates passive paracellular diffusion of calcium in intestine. This local adaptation adjusts the fractional calcium absorption according the body requirement. Failure of local adaptation due to decreased calcium intake, decreased supply of 25OHD, mutation in CaSR or vitamin D system decreases systemic calcium levels and systemic adaptations comes into the play. Systemic adaptations consist of rise in PTH and increase in active vitamin D metabolites. These adaptations lead to bone resorption and maintenance of calcium homeostasis. Not all subjects with varying levels of VDD manifest with secondary hyperparathyroidism and decreased in bone mineral density. We suggest that rise in PTH is first indicator of VDD is rise in PTH along with decrease in BMD depending on duration of VDD. Hence, subjects with any degree of VDD with normal PTH and BMD should not be labeled as vitamin D deficient. These subjects can be called subclinical VDD, and further studies are required to assess beneficial effect of vitamin D supplementation in this subset of population. This hypothesis further highlights pitfalls in treatment of hypoparathyroidism.
    Medical Hypotheses 05/2013; 81(2). DOI:10.1016/j.mehy.2013.04.035 · 1.07 Impact Factor
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