Persistence of severe iodine-deficiency disorders despite universal salt iodization in an iodine-deficient area in northern India.

OBJECTIVE: The aim of the present study was to determine the impact of universal salt iodization (USI) on the prevalence of iodine deficiency in the population of an area previously known to have severe iodine deficiency in India. DESIGN: In a cross-sectional survey, a total of 2860 subjects residing in fifty-three villages of four sub-districts of Gonda District were examined for goitre and urinary iodine concentration. Free thyroxine and thyroid-stimulating hormone levels were also measured. Salt samples from households were collected for estimation of iodine content. RESULTS: A reduction in goitre prevalence was observed from 69 % reported in 1982 to 27.7 % assessed in 2007. However, 34 % of villages still had very high endemicity of goitre (goitre prevalence >30 %). Twenty-three per cent of households consumed a negligible amount (<5 ppm) and 56 % of households consumed an insufficient amount (5-15 ppm) of iodine from salt. CONCLUSIONS: Although there was an overall improvement in iodine nutrition as revealed by decreased goitre prevalence and increased median urinary iodine levels, there were several pockets of severe deficiency that require a more targeted approach. Poor coverage, the use of unpackaged crystal salt with inadequate iodine and the washing of salt before use by 90 % of rural households are the major causes of persisting iodine-deficiency disorders. This demonstrates lapses in USI implementation, lack of monitoring and the need to identify hot spots. We advocate strengthening the USI programme with a mass education component, the supply of adequately iodized salt and the implementation of complementary strategies for vulnerable groups, particularly neonates and lactating mothers.

Calcium deficiency-induced secondary hyperparathyroidism and osteopenia are rapidly reversible with calcium supplementation in growing rabbit pups.

The reversibility of osteopenia secondary to isolated Ca deficiency (CaDef) is still not clear. We studied the effect of severe CaDef on Ca homeostasis and bone accrual in a 'hypercalcaemic' animal, the rabbit, during the post-weaning period and its reversibility on Ca supplementation. Male Belgian 5-week-old rabbit pups were fed CaDef diet (0.026 % Ca) for 10 weeks. As compared with those fed with a normal chow diet (0.45 % Ca), CaDef pups developed significant hypocalcaemia (P < 0.05), hypocalciuria (urinary Ca 76 (SEM 12) v. 17 (SEM 1) mg/l; P < 0.005), hypophosphataemia (serum inorganic P 100 (SEM 6) v. 65 (SEM 4) mg/l; P < 0.005), secondary hyperparathyroidism (SHPT) (serum intact parathyroid hormone human equivalent 18.2 (SEM 1.4) v. 125.0 (SEM 4.5) pg/ml; P < 0.001) and elevated serum calcitriol levels (34.0 (SEM 3.9) v. 91.0 (SEM 1.0) pg/ml; P < 0.005). Elevated urinary C-terminal telopeptide of class I collagen (P < 0.005) and total serum alkaline phosphatase (P < 0.005) suggested increased bone turnover. There was a significantly lower gain in bone mineral density (BMD) and bone mineral content (BMC) in the whole body and lumbar spine in vivo, and various sub-regions of the femur and tibia in vitro. Supplementation of adequate Ca (0.45 % Ca) after 15 weeks on the normal diet resulted in rapid catch-up growth, and resolution of SHPT. Rapid gain in various BMD and BMC parameters continued at 30 weeks of age, and both were comparable with those in rabbits on a normal diet. We conclude that Ca deficiency-induced SHPT and poor bone accrual in growing rabbit pups are rapidly reversible with Ca supplementation. The present study indicates that early intervention may be a more appropriate window period for human nutritional corrective measures.

High prevalence of vitamin D deficiency among pregnant women and their newborns in northern India.

BACKGROUND: Vitamin D deficiency is prevalent in India, a finding that is unexpected in a tropical country with abundant sunshine. Vitamin D deficiency during pregnancy has important implications for the newborn and infant. There are few data from India about the prevalence of hypovitaminosis D in pregnancy and in the newborn. OBJECTIVE: Our aim was to determine the prevalence of osteomalacia and hypovitaminosis D in pregnancy and in cord blood and to correlate maternal 25-hydroxyvitamin D [25(OH)D] status with sun exposure, daily calcium intake (dietary plus supplemental), and intact parathyroid hormone (PTH) concentrations. DESIGN: Serum calcium, inorganic phosphorus, 25(OH)D, heat-labile alkaline phosphatase, and PTH were studied in 207 urban and rural pregnant subjects at term. Alkaline phosphatase and 25(OH)D were measured in the cord blood of 117 newborns. RESULTS: Mean maternal serum 25(OH)D was 14 +/- 9.3 ng/mL, and cord blood 25(OH)D was 8.4 +/- 5.7 ng/mL. PTH rose above the normal range when 25(OH)D was <22.5 ng/mL. Eighty-four percent of women (84.3% of urban and 83.6% of rural women) had 25(OH)D values below that cutoff. Fourteen percent of the subjects had elevated alkaline phosphatase (17% of urban and 7% of rural subjects). Calcium intake was uniformly low, although higher in urban (842 +/- 459 mg/d) than in rural (549 +/- 404 mg/d) subjects (P < 0.001). Maternal serum 25(OH)D correlated positively with cord blood 25(OH)D (r = 0.79, P < 0.001) and negatively with PTH (r = -0.35, P < 0.001). CONCLUSION: We observed a high prevalence of physiologically significant hypovitaminosis D among pregnant women and their newborns, the magnitude of which warrants public health intervention.