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Indian Pediatr 2010;47:
755-756 |
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Vitamin D Deficiency in Indian Adolescents |
AV Khadilkar
Growth and Pediatric Endocrine Research Unit, Hirabai
Cowasji Jehangir Medical Research Institute, Jehangir Hospital,
32, Sassoon Road, Pune 411 001, India.
Email:
[email protected]
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In humans, the main source of vitamin D
comes from photoconversion of 7-dehydrocholesterol in the skin to
cholecalciferol (vitamin D3) by solar ultraviolet radiation (UVB: 290-320
nm). Vitamin D formed in the skin or the small amount absorbed from the
diet is hydroxylated at the 25 position to produce 25 hydroxyvitamin D
(25OHD), which is considered to be a reliable index of an individual’s
vitamin D status. Vitamin D is crucial for calcium homeostasis and
musculoskeletal health. Adequate vitamin D status during adolescence might
help to reduce the risk of osteoporotic fractures in later life. There is
also a growing body of evidence linking vitamin D status with non-skeletal
disorders including autoimmune disorders (Crohn’s disease, multiple
sclerosis, rheumatoid arthritis, and type 1 diabetes), infections, and
risk of developing cancers of the breast, colon, prostate and ovaries(1).
It is intriguing as to why vitamin D deficiency is such
a common problem among Indians inspite of abundant sunshine. For example,
we found vitamin D status of adolescent girls in Pune (latitude 18.34º N)
was similar to that of adolescent girls in Manchester, UK (latitude 53.4 º
N), assessed during an equivalent season(2). This was probably because
Pune girls had very low calcium intake and a high fibre diet which may
have led to a depletion of body stores of vitamin D. Other reasons may be
genetic factors. For example, South Asians have increased
25(OH)D-24-hydroxylase, which degrades 25(OH)D to inactive metabolites(3).
More recently, it has been shown that the increment in serum 25OHD in
response to treatment depends on the heritability of vitamin D binding
protein(4).
While there is no consensus on definitions of vitamin D
deficiency and sufficiency, serum concentrations of <50 nmol/L are
considered to be the lower acceptable level by Lawson Wilkins Pediatric
Endocrine Society in the USA(5). In spite of widespread vitamin D
deficiency, it is surprising that the Indian Council of Medical Research,
even in its current updated guidelines does not give any specific
recommendations for Vitamin D intake, as it is believed that we Indians
get sufficient Vitamin D from sunlight.
The study by Marwah and colleagues(6) published in this
issue of Indian Pediatrics has shown that adolescents in Delhi from
upper and lower socioeconomic groups had mean serum 25OHD concentration of
31 nmol/L. The authors also found that despite supplementation with 60,000
IU of Vitamin D3 (monthly 2000 IU/day or two-monthly 1000 IU/day, only 47%
subjects were vitamin D sufficient at the end of one year (mean 25OHD
level 50.1 nmol/L). These varied responses to supplementation
suggest that perhaps the response to supplementation may also be
attributed to other factors known to affect vitamin D levels such as
season, ethnicity, calcium intake, body mass index, physical activity,
pollution and skin color.
Marwah, et al.(6) have also found that post-
supplementation, serum parathyroid hormone (PTH) values have increased
above the baseline levels particularly in the lower socio economic
stratum, inspite of increment in serum 25OHD concentration. This was a
surprising finding and is difficult to explain. Possible explanations
include very low dietary calcium to phosphorous ratio in adolescents from
the lower socioeconomic group, high dietary phosphorous may have acted as
a potent stimulant to the parathyroid glands, and this rise in PTH was
possibly not overcome by the post-supplementation increment in serum
25OHD. We have also shown that low dietary calcium intake can result in
raised serum PTH concentrations due to reversible end organ resistance to
the actions of PTH(7).
It is becoming increasingly evident that abundant
sunshine does not seem to protect Indians from widespread biochemical
vitamin D deficiency. Hopefully, results of this important trial will
stimulate further research to determine the genetic and environmental
factors which are responsible for low serum 25OHD values in India, and the
optimum vitamin D treatment regimens that are necessary to rectify low
body stores of vitamin D among Indian children.
Funding: None.
Competing interests: None.
References
1. Holick MF. Vitamin D deficiency. N Engl J Med 2007;
357: 266-281.
2. Khadilkar A, Das G, Sayyad M, Sanwalka N, Bhandari
D, Khadilkar V, et al. Low calcium intake and hypovitaminosis D in
adolescent girls. Arch Dis Child 2007; 92: 1045.
3. Awumey EM, Mitra DA, Hollis BW, Kumar R, Bell NH.
Vitamin D metabolism is altered in Asian Indians in the southern United
States: a clinical research center study. J Clin Endocrinol Metab 1998;
83: 169-173.
4. Fu L, Yun F, Oczak M, Wong BY, Vieth R, Cole DE.
Common genetic variants of the vitamin D binding protein (DBP) predict
differences in res-ponse of serum 25-hydroxyvitamin D [25(OH)D] to vitamin
D supplementation. Clin Biochem 2009; 42: 1174-1177.
5. Misra M, Pacaud D, Petryk A, Collett-Solberg PF,
Kappy. Vitamin D deficiency in children and its management: review of
current knowledge and recommendations. Pediatrics 2008; 122: 398-417.
6. Marwaha R, Tandon N, Agarwal N, Puri S, Agarwal R,
Singh S, et al. Impact of two regimens of vitamin D supplementation
on calcium - vitamin D - PTH axis of schoolgirls of Delhi. Indian Pediatr
2010; 47: 761-769.
7. Khadilkar A, Mughal MZ, Hanumante N, Sayyad M,
Sanwalka N, Naik S, et al. Oral calcium supplementation reverses
the biochemical pattern of parathyroid hormone resistance in
under-privileged Indian toddlers. Arch Dis Child 2009; 94: 932-937.
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