VITAMIN-D DEFICIENCY IN ASIANS AT HOME AND IN BRITAIN
Abstract
Serum concentrations of calcium, inorganic phosphorus, and alkaline phosphatase were measured in 119 Indians living in or around the Punjab town of Ludhiana. In contrast to the findings in an earlier survey among an ethnically similar group of Asians living in northern England, biochemical evidence suggesting the presence of vitamin-D deficiency was found in only one Punjabi. Since the intake of vitamin D was low and the dietary and social customs were similar in the two groups, it is inferred that the absence of vitamin-D deficiency in the Punjabis was probably due to their exposure to sunshine. It is concluded that the high frequency of rickets and osteomalacia among Asians in Britain can be explained by their low intake of vitamin D and inadequate solar exposure. This conclusion accords fully with the results of earlier epidemiological studies of the frequency of these diseases in the Indian subcontinent.
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Cited by (63)
Vitamin D deficiency and nutritional rickets in infants and children
2023, Feldman and Pike's Vitamin D: Volume Two: Disease and TherapeuticsNutritional rickets remains a global public health problem, despite effective and inexpensive methods to prevent and treat the disease. It is most prevalent in the infant/toddler age groups and the adolescent, but vitamin D deficiency is also prevalent in women of child-bearing age, resulting in babies being born with low vitamin D stores and the mothers having inadequate vitamin D in breast milk, thus exacerbating the risk for rickets in these infants. In the very-low-birth-weight infant, low dietary phosphorus intake also plays a role in the development of the metabolic bone disease of prematurity. In a number of subtropical developing countries, rickets appears to be due to low dietary calcium intakes (approximately 200 mg/day) rather than vitamin D deficiency. Biochemically, these children are differentiated from those with vitamin D deficiency by having markedly elevated serum 1,25(OH)2D concentrations and high fractional intestinal calcium absorption. Nutritional rickets represents the outcome of a spectrum of causes, ranging from vitamin D deficiency on one hand to dietary calcium deficiency on the other, while in between low dietary intakes and vitamin D insufficiency act synergistically to increase the risk of developing the disease.
Reduced Maternal Serum Total, Free and Bioavailable Vitamin D Levels and its Association with the Risk for Postpartum Depressive Symptoms
2021, Archives of Medical ResearchCitation Excerpt :Majority of the cases (61%) and controls (77%) were studied in winter (September–March with relatively low sun exposure) 39% of cases and 22% of controls in summer (April–August) respectively based on the regional climate (24). Further, it is assumed that residing in tropical country with abundant sunshine favours enough cutaneous vitamin D synthesis throughout the year (25). The suicide risk was evaluated by examining response to the item no.10 of the EPDS (26).
Low vitamin D levels have been implicated in postpartum depressive disorders. However, studies on bioavailable vitamin D levels in postpartum depression are limited. Our study aimed to assess the serum concentrations of total, free and bioavailable 25-hydroxyvitamin D (25(OH)D) levels in women with postpartum depressive symptoms (PPD) and the association between 25(OH)D levels and PPD at 6 week post-delivery.
In this cross-sectional study, a total of 330 cases and 330 age and BMI matched controls were recruited from the tertiary care hospital in South India. Women with depressive symptoms were assessed using the validated Edinburg Postnatal Depression Scale (EPDS) and cut-off score ≥10 was used. Serum 25(OH)D and VDBP levels were measured using commercially available ELISA kits.
Serum total, free and bioavailable 25(OH)D levels were significantly lower in postpartum depressive women compared to non-depressive women (p <0.001, p = 0.01). A significant negative correlation was observed between 25(OH)D, free 25(OH)D and bioavailable 25(OH)D with EPDS score in total study subjects (p <0.001, r = −0.19; p <0.001, r = −0.14 and p <0.001, r = −0.14). Multivariate linear regression analysis further confirmed a significant association between serum total, free and bioavailable 25(OH)D levels and EPDS score (p <0.001∗).
Our study demonstrated that lower serum total, free and bioavailable 25(OH)D levels were associated with postpartum depressive symptoms. Hypovitaminosis D after delivery may be a risk factor for postpartum depression.
Nutritional Rickets
2012, Pediatric BoneThis chapter reviews the general features of rickets, classification of the various causes of the disease, and nutritional rickets. Rickets is a clinical syndrome characterized by a failure of or delays in endochondral calcification at the growth plates of long bones, resulting in deformation of the growth plate, a reduction in longitudinal growth and the development of bone deformities. The disease is also associated with osteomalacia, which is a failure of mineralization of preformed osteoid on the trabecular and cortical bone surfaces of all bones. Rickets has been a public health problem for children living in temperate climates for many centuries. The causes of rickets may be divided into three major categories based on their pathogenetic mechanisms. Normal mineralization of the growth plate and of osteoid at the trabecular and cortical bone surfaces is dependent on a number of different factors, including the presence of normal concentrations of both calcium and phosphorus, and of alkaline phosphatase. The classification helps to categorize the causes into broad groups, each of which has characteristic biochemical changes, which help in establishing the pathogenesis of the disease in an individual child. In the calciopenic forms of rickets, the typical biochemical changes include hypocalcemia and hyperparathyroidism, while in the phosphopenic form, hypophosphatemia with normal parathyroid hormone concentrations are characteristic and in many situations associated with elevated fibroblast growth factor 23 (FGF-23) concentrations.
Nutritional Rickets
2011, Pediatric Bone: Biology and DiseasesThis chapter reviews the general features of rickets, classification of the various causes of the disease, and nutritional rickets. Rickets is a clinical syndrome characterized by a failure of or delays in endochondral calcification at the growth plates of long bones, resulting in deformation of the growth plate, a reduction in longitudinal growth and the development of bone deformities. The disease is also associated with osteomalacia, which is a failure of mineralization of preformed osteoid on the trabecular and cortical bone surfaces of all bones. Rickets has been a public health problem for children living in temperate climates for many centuries. The causes of rickets may be divided into three major categories based on their pathogenetic mechanisms. Normal mineralization of the growth plate and of osteoid at the trabecular and cortical bone surfaces is dependent on a number of different factors, including the presence of normal concentrations of both calcium and phosphorus, and of alkaline phosphatase. The classification helps to categorize the causes into broad groups, each of which has characteristic biochemical changes, which help in establishing the pathogenesis of the disease in an individual child. In the calciopenic forms of rickets, the typical biochemical changes include hypocalcemia and hyperparathyroidism, while in the phosphopenic form, hypophosphatemia with normal parathyroid hormone concentrations are characteristic and in many situations associated with elevated fibroblast growth factor 23 (FGF-23) concentrations.
Vitamin D deficiency and nutritional rickets in children
2011, Vitamin D: Two-Volume SetRickets is a clinical syndrome that occurs in children as a result of a failure of or delay in mineralization of the growth plate of growing bones. There are numerous causes, the majority of which can be grouped into three major categories—those which primarily result in a failure to maintain normal calcium homeostasis; those which primarily affect phosphate homeostasis; and those which directly inhibit the mineralization process. Globally, rickets due to nutritional causes remains the most frequent form of the disease seen. Despite readily accessible and effective means to eradicate rickets globally, the disease remains a major public health problem in many countries, not only in temperate regions of the world but also in tropical and subtropical countries. In many developed countries, the promotion of exclusive breast-feeding during the first six months of life and the concerns about the long-term effect of sunlight exposure during this period have exacerbated the risks of vitamin D deficiency in the young infant. In some subtropical countries, social customs play an important role in preventing adequate vitamin D status not only in the young infant but also in the pregnant and lactating mother. In a number of developing countries, low dietary calcium intakes appear to play a major role in the pathogenesis of rickets in older children. Recent studies have helped to provide an all-embracing concept of the interaction of vitamin D and calcium intakes in the pathogenesis of rickets.
Vitamin D deficiency and nutritional rickets in children
2011, Vitamin DRickets is a clinical syndrome that occurs in children as a result of a failure of or delay in mineralization of the growth plate of growing bones. There are numerous causes, the majority of which can be grouped into three major categories—those which primarily result in a failure to maintain normal calcium homeostasis; those which primarily affect phosphate homeostasis; and those which directly inhibit the mineralization process. Globally, rickets due to nutritional causes remains the most frequent form of the disease seen. Despite readily accessible and effective means to eradicate rickets globally, the disease remains a major public health problem in many countries, not only in temperate regions of the world but also in tropical and subtropical countries. In many developed countries, the promotion of exclusive breast-feeding during the first six months of life and the concerns about the long-term effect of sunlight exposure during this period have exacerbated the risks of vitamin D deficiency in the young infant. In some subtropical countries, social customs play an important role in preventing adequate vitamin D status not only in the young infant but also in the pregnant and lactating mother. In a number of developing countries, low dietary calcium intakes appear to play a major role in the pathogenesis of rickets in older children. Recent studies have helped to provide an all-embracing concept of the interaction of vitamin D and calcium intakes in the pathogenesis of rickets.