Article

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

ABSTRACT 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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Available from: Shashank Joshi, May 29, 2014
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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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    • "Prevalence of VDD was shown to be 76% and 70% respectively among women of reproductive and postmenopausal-age groups in South India (Harinarayan et al., 2011). Several studies indicate that VDD is very common among males and females of all age groups in India (Harinarayan & Joshi, 2009; Marwaha & Sripathy, 2008). Many groups of researchers have reported 16.5% of women of reproductive age group to be affected with VDD in South India and the prevalence was estimated to be about 84% among pregnant women in North India (Harinarayan et al., 2011; Marwaha et al., 2011; Sachan et al., 2005). "
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    ABSTRACT: This article provides a comprehensive review of the extent of prevalence of micronutrient deficiencies (vitamin A & D, iron, zinc and iodine) among different population groups in India, Pakistan, Bangladesh and Sri Lanka. The article also covers several health implications associated with these deficiencies, their economic impact and numerous strategies to combat this issue in low income South Asian countries. An extensive computer-based bibliographic review of the literature was performed via PubMed, Web of Science, Scopus, and Google Scholar by using keywords “micronutrients”, “vitamin A and D”, “iron”, “zinc”, “iodine” and “South Asia”. Data were identified under various sections and the most relevant full-text articles and abstracts were selected and screened for inclusion in this review. The results indicate that micronutrient deficiencies are widely prevalent in these regions and are now a significant public health problem. Preschool-age and school children, pregnant women and women of childbearing age are at the risk of these deficiencies. Vitamin A deficiency (VAD) was found among school-age children and adolescents in Bangladesh and Sri Lanka. Vitamin D deficiency (VDD) seemed to affect 84% of pregnant women in India, 70% of healthy volunteers in Pakistan, 26% of male children in Sri Lanka and 8% of children in Bangladesh. Data illustrate that iron deficiency anemia (IDA), zinc and iodine deficiency affect all population groups, suggesting immediate measures to be taken to address the issue. Restricted dietary intake of these nutrients associated with a number of socioeconomic constraints exacerbates the problem of micronutrient malnutrition. Dietary diversification, food fortification and supplementation are the pragmatic and recommended approaches to overcome these nutritional deficiencies. However, the goal to virtually eliminate micronutrient deficiencies in these poorer societies demands a series of well integrated actions at all levels
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    ABSTRACT: Chronic antiepileptic drug use is associated with bone loss. We sought to assess the longitudinal effect of antiepileptic drug on serum 25-hydroxyvitamin D [25(OH)D] levels and bone mineral metabolism markers. Patients in the emergency services or those in neurology outpatient department with history of seizure were characterized and included in the study prospectively. Daily dietary intake of calories, calcium, phosphorus and phytates were characterized by dietary recall method. Base line bone mineral parameters - serum calcium, phosphorus, alkaline phosphatase (SAP), tartrate resistant acid phosphatase (TRACP), 25(OH)D levels, parathyroid hormone (PTH) and urinary calcium creatinine ratio (Ca.Cr), urinary calcium/kg/bodyweight (BW) and phosphate excretion index (PEI) were determined. Patients on AED therapy with normal 25(OH)D levels were followed up and were re-evaluated at the end of 6 months. The daily dietary calcium intake of the subjects was lower than the RDA (Recommended Dietary Allowance) by ICMR (Indian Council of Medical Research). The diet was high in phytates. Two-thirds of the recruited subjects were vitamin D deficient. Subjects with normal 25(OH)D levels at base line showed a significant fall of 25(OH)D levels, urinary calcium, urinary calcium/kg/BW and TRACP levels at the end of 6 months irrespective of the AED used or the plasma level of AED. Hypovitaminosis D is common in our population. Subjects with normal 25(OH)D levels, irrespective of the type of antiepileptic medications even at sub-therapeutic serum levels of the drug, went into 25(OH)D deficiency and insufficiency states. Theoretically it can be worthwhile to supplement calcium and vitamin D even before initiation of antiepileptic therapy.
    Seizure 02/2010; 19(3):153-8. DOI:10.1016/j.seizure.2010.01.006 · 2.06 Impact Factor
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