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Community and International Nutrition

Season and Ethnicity Are Determinants of Serum 25-Hydroxyvitamin D Concentrations in New Zealand Children Aged 5–14 y^1,2

Jennifer E. Rockell^*, Timothy J. Green^*,3, C. Murray Skeaff^*, Susan J. Whiting, Rachael W. Taylor^*, Sheila M. Williams^**, Winsome R. Parnell^*, Robert Scragg, Noela Wilson, David Schaaf, Eljon D. Fitzgerald and Mark W. Wohlers

^* Department of Human Nutrition LINZ Activity and Health Research Unit and ^** Preventive and Social Medicine, University of Otago, Dunedin, New Zealand; College of Pharmacy and Nutrition, University of Saskatchewan, Saskatoon, Saskatchewan, Canada; School of Population Health, Faculty of Medicine and Health Science, University of Auckland, Auckland, New Zealand; and School of Mori Studies, Massey University, Palmerston North, New Zealand

³To whom correspondence should be addressed. E-mail: tim.green{at}stonebow.otago.ac.nz.

	ABSTRACT

TOP ABSTRACT SUBJECTS AND METHODS RESULTS DISCUSSION LITERATURE CITED

 
New Zealand children, particularly those of Mori and Pacific ethnicity, may be at risk for low vitamin D status because of low vitamin D intakes, the country’s latitude (35–46°S), and skin color. The aim of this study was to determine 25-hydroxyvitamin D concentrations and their determinants in a national sample of New Zealand children aged 5–14 y. The 2002 National Children’s Nutrition Survey was designed to survey New Zealand children, including oversampling of Mori and Pacific children to allow ethnic-specific analyses. A 2-stage recruitment process occurred using a random selection of schools, and children within each school. Serum 25-hydroxyvitamin D concentration [mean (99% CI) nmol/L] in Mori children (n = 456) was 43 (38,49), in Pacific (n = 646) 36 (31,42), and in New Zealand European and Others (NZEO) (n = 483) 53 (47,59). Among Mori, Pacific, and NZEO, the prevalence (%, 99% CI) of serum 25-hydroxyvitamin D deficiency (<17.5 nmol/L) was 5 (2,12), 8 (5,14), and 3 (1,7), respectively. The prevalence of insufficiency (<37.5 nmol/L) was 41 (29,53), 59 (42,75), and 25 (15,35), respectively. Multiple regression analysis found that 25-hydroxyvitamin D concentrations were lower in winter than summer [adjusted mean difference (99% CI) nmol/L; 15 (8,22)], lower in girls than boys [5 (1,10)], and lower in obese children than in those of "normal" weight [6 (1,11)]. Relative to NZEO, 25-hydroxyvitamin D concentrations were lower in Mori [9 (3,15)] and Pacific children [16 (10,22)]. Ethnicity and season are major determinants of serum 25-hydroxyvitamin D. There is a high prevalence of vitamin D insufficiency in New Zealand children, which may or may not contribute to increased risk of osteoporosis and other chronic disease. There is a pressing need for more convincing evidence concerning the health risks associated with the low vitamin D status in New Zealand children.

KEY WORDS: • 25-hydroxyvitamin D • children • New Zealand • Mori • Pacific

Vitamin D plays an essential role in calcium and phosphorus homeostasis. The most serious clinical consequence of vitamin D deficiency in children is rickets, a condition characterized by soft and weakened bones, resulting from poor mineralization of newly formed bone tissue (1). Although still uncommon in Western countries, it would appear from the increasing number of case reports being published that rickets is reemerging as a public health problem (2–4). Lesser degrees of vitamin D deficiency, often referred to as insufficiency, are associated with lower bone mineral density (BMD)⁴ (5) and bone accretion rates in children (6), as well as elevated serum parathyroid (PTH) hormone concentrations (5,7); these effects are consistent with secondary hyperparathyroidism. Recent discoveries indicate that vitamin D has functions unrelated to calcium, specifically in cell differentiation and in the immune system (8,9). These biological effects add plausibility to reports that low vitamin D status is associated with increased risk of childhood-onset Type 1 diabetes (10) and increased risk of some types of cancer in adults (11–13).

This widening spectrum of diseases in which vitamin D may play an etiological role and the reemergence of rickets give greater relevance and priority to monitoring the vitamin D status of populations, particularly children. The best indicator of vitamin D status is the concentration of circulating 25-hydroxyvitamin D. The determinants of serum 25-hydroxyvitamin D concentrations in children include dietary vitamin D intake, which in the absence of fortified foods or supplements is generally low, and conditions that affect the synthesis of vitamin D in the skin such as skin color and sun exposure; the latter are affected by season, geographic latitude, sunscreen use, and clothing (1). Obesity has been associated with lower vitamin D status in adults (14,15), an effect that may be stronger in young than older adults (16). The effect of obesity on the vitamin D status of children is not clear.

There have been several community or clinic-based studies of the vitamin D status of children (5,17–23), but few studies have reported vitamin D status of a nationally representative group of children (24,25). Results from the 3rd U.S. National Health and Nutrition Examination Survey (NHANES III) indicated that the prevalence of insufficient serum 25-hydroxyvitamin D (<37.5 nmol/L) in the 12- to 19-y-old U.S. population ranged from 2 to 12%, although this is likely to be an underestimate because vitamin D status was measured in the northern United States during summer and in the southern United States during winter. These rates prevail despite the widespread fortification of milk and breakfast cereals in the United States (18,24).

We present the serum 25-hydroxyvitamin D results from the Children’s Nutrition Survey (CNS02), a large national survey of New Zealand school-aged children in 2002. The vitamin D analysis was initiated in response to evidence from Tasmania, Australia (42°S) that there was a high prevalence of low vitamin D status among children and adolescents (17). New Zealand lies geographically from 35°S to 47°S (equivalent to Duluth, MN, and Los Angeles, CA) and has a food supply with no mandatory and minimal voluntary vitamin D (some margarines and some edible fat spreads) fortification. Furthermore, there are 3 main ethnic groups with varying skin color: Mori, Pacific, and New Zealand European. Moreover, the survey provides a unique opportunity to explore the independent effects of season, age, ethnicity, and obesity on serum 25-hydroxyvitamin D concentrations in children 5–14 y old.

	SUBJECTS AND METHODS

TOP ABSTRACT SUBJECTS AND METHODS RESULTS DISCUSSION LITERATURE CITED

 
    Study design and population. The 2002 National Children’s Nutrition Survey (CNS02) was a cross-sectional survey of a national sample of New Zealand school children and adolescents aged 5 to 14 y, conducted during the 2002 school year. A school-based sampling frame of children was used with oversampling of Mori and Pacific children to allow for ethnic-specific analysis. The CNS02 aimed to recruit 3000 children with 1000 from each of 3 ethnic groups: Mori, Pacific, and New Zealand Europeans and Others (NZEO). After exclusion of some schools for reasons of cost (schools on the Chatham Islands, correspondence schools, and schools with <50 students), 160 schools were randomly selected from Ministry of Education rolls. Because 16 schools declined to participate, a further sample of 30 schools was selected, with 2 schools declining. The final sample was selected from 172 schools. Recruitment from each school was in proportion to the number of students on the school roll. Children from selected schools were assigned to 1 of 3 ethnic groups with a different probability of selection for each ethnic group. Details of the survey methodology are described more fully elsewhere (26). Although the survey sample covered rural and urban areas across New Zealand, blood samples were not collected from rural areas due to concerns about blood stability and cost. The total number of children invited to participate was 4728; of these, 3275 participated and 1927 provided blood samples. Blood was available for vitamin D analysis for 1659 participants. Of these, 1585 children had all data available that were relevant to this study, yielding an overall response rate of 33.5%. The survey received ethical approval from the Auckland Ethics Committee. Informed written consent was obtained from both the children and their parents or guardians.

Demographic data were obtained from interviews, at children’s homes in the presence of their parents or guardians, although some took place at school. Interviews were conducted from the last week of February 2002 through the second week of December 2002. In this paper, the term "Pacific" includes children who identify as Samoan (55%), Tongan (24%), Cook Island Mori (16%), Niuean (10%), Tokelauan (2%), Fijian (3%), and other Pacific ethnic groups (3%). The New Zealand European and Others (NZEO) group included: New Zealand European (80%), Asian (10%), Other European (6%), Indian (5%), and other (4%). In cases in which the child or parent/guardian indicated that they belonged to more than one ethnic group, a single ethnic category was assigned to the child using a priority system as follows: if Mori was one of the groups reported, the participant was assigned to Mori. If Mori was not reported, but any of the Pacific groups were reported, the participant was assigned to Pacific. All remaining participants were assigned to NZEO.

Anthropometric measurements and blood samples were taken at each child’s school. Height and weight measurements were taken using portable standardized equipment. BMI was calculated as weight in kilograms divided by height in meters squared. Prevalences of overweight and obesity were determined using the reference cutoff values of Cole et al. (27). Blood samples were collected by trained phlebotomists. The children were not instructed to fast. Blood was drawn from an antecubital vein into vacuum-evacuated tubes. Blood samples were centrifuged (2500 x g, 7 min), the serum was removed, and put into cryovials; surplus blood was stored at –80°C for subsequent analyses. The samples underwent no freeze-thaw cycles and were stored for up to 18 mo before being analyzed for 25-hydroxyvitamin D.

    Serum 25-hydroxyvitamin D analysis. Serum 25-hydroxyvitamin D was determined on surplus blood using an RIA kit (DiaSorin) that recognizes both cholecalciferol and ergocalciferol equally and measures total 25-hydroxycholecalciferol (25-hydroxyvitamin D). Two levels of control provided by the manufacturer were run in each assay. Inter- and intra-assay CVs based on repeated analysis of a pooled control were 13 and 9%, respectively. The sensitivity of the assay is 7 nmol/L. Certified reference material for serum 25-hydroxyvitamin D is not available; however, to verify the relative accuracy of our results, we sent aliquots of 20 randomly selected samples to the Steroid Laboratory of Canterbury Health Laboratories. This laboratory, using the same method, reported a mean serum 25-hydroxyvitamin D concentration of 51 nmol/L, compared with our measured mean of 53 nmol/L. Using a paired t test, the difference was [mean (95% CI)] 1.7 (–4.2, 7.5). The Bland and Altman test showed the 95% limits of agreement were –23.4, 26.7.

    Data analysis. Statistical analyses were carried out using STATA 8.0, adjusting for the complex survey design. Tests for independence were used to examine the association between those who did and did not give blood and demographic variables such as gender and ethnicity. The ² statistic was corrected for the survey design and converted into an F-statistic. Sampling weights were used in all analyses to obtain unbiased estimates of population serum vitamin D concentrations. Sampling weights were based on the provision of a blood sample rather than participation in the survey because only children from urban areas were sampled for blood. Sample weights were based on the inverse probability of selection, and adjusted for differential nonresponse and poststratification by age, sex, and ethnicity. Because age, sex, ethnicity, season, geographical location, and obesity were reported to affect serum 25-hydroxyvitamin D concentrations, we used multiple linear regression models to examine the independent relations between each of these variables and serum 25-hydroxyvitamin D. We estimated adjusted means based on these models. Because the prevalence of deficiency was <10%, Poisson regression was used to estimate the prevalence (99% CI) for the groups of interest. Logistic regression was used for estimating prevalence of insufficiency. For the purposes of analysis, the months of April through September were defined as "winter" months, and October to December, and March, defined as "summer" months. We used Poisson regression to identify characteristics predicting risk of vitamin D deficiency (serum 25-hydroxyvitamin D < 17.5 nmol/L) and logistic regression for predictors of risk insufficiency (<37.5 nmol/L) so that relative risks (for Poisson) and odds ratios were obtained. There were no significant interactions in the multivariate regression models. Estimates were considered significant if P < 0.01.

	RESULTS

TOP ABSTRACT SUBJECTS AND METHODS RESULTS DISCUSSION LITERATURE CITED

 
Characteristics of the children for whom a serum 25-hydroxyvitamin D concentration was obtained (n = 1585) were compared with those of all participants in the Children’s Nutrition Survey (n = 3275) (Table 1). The distribution of sex, age, season, and overweight or obese did not differ between these groups. The vitamin D subgroup comprised only children from urban schools, and there were greater proportions of Pacific (² = 60.7, P = 0.0002) and North Island (² = 95.5, P = 0.0005) children than in the survey group.

View larger version (16K): [in this window] [in a new window]   FIGURE 1 Serum 25-hydroxyvitamin D concentrations by month, of New Zealand children and adolescents (n = 1583) who participated in the 2002 National Children’s Nutrition Survey. Values are means (99% CI) adjusted for age, sex, ethnicity, latitude, and obesity using multiple linear regression, and weighted to account for the complex survey design. *Different from March, P < 0.01.

	DISCUSSION

TOP ABSTRACT SUBJECTS AND METHODS RESULTS DISCUSSION LITERATURE CITED

 
We found that 1 in 25 (4%) New Zealand children aged 5–14 y had a serum 25-hydroxyvitamin D concentration low enough (<17.5 nmol/L) to be classified as vitamin D deficient and 31% as insufficient (<37.5 nmol/L). Vitamin D deficiency in children is generally defined as a concentration of serum 25-hydroxyvitamin D below which there is overt evidence of compromised skeletal health such as the presence of rickets, most common in infancy and at puberty, other radiological evidence of poor bone development, or marked biochemical abnormalities associated with metabolic bone disease (28). Cutoff values indicative of vitamin D deficiency in children, based on 25-hydroxyvitamin D, range from 10 to 25 nmol/L (1,21). A cutoff value of 17.5 nmol/L was used to define vitamin D deficiency, in adolescents and adults in the U.S. NHANES III (24).

There is a continuum of increasing risk of compromised growth and development in children as serum 25-hydroxyvitamin D concentration decreases from sufficiency to deficiency. Although there is no current consensus on the optimal definition of vitamin D insufficiency, studies (primarily of older adults) suggest that higher serum 25-hydroxyvitamin D concentrations (50–80 nmol/L) (29) may be necessary to prevent secondary hyperparathyroidism (30–32), increased bone loss (33), or fracture (34) and to maximize fractional calcium absorption (35). Because older people tend to have a reduced capacity for intestinal calcium absorption (36) and may be more resistant to vitamin D than children, applying adult cutoff values to children and adolescents may be inappropriate.

Health indicators used to define vitamin D insufficiency in children include minimization of PTH concentrations and maximization of bone mass. Estimates of the serum 25-hydroxyvitamin D concentration indicative of insufficiency in children based on suppression of PTH range from 30 to 83 nmol/L (5,19,22). Defining vitamin D insufficiency by PTH suppression should be interpreted with caution because at higher calcium intakes, absorption of calcium is sufficient to maintain normal serum calcium and PTH is not elevated. The daily calcium intake of New Zealand children (mean ± SEM) was 767 ± 13 mg; however, in Pacific children, it was 558 ± 28 mg. Achieving peak bone mass during childhood is important for the prevention of osteoporosis later in life. Vitamin D insufficiency during childhood may limit the attainment of peak bone mass (37), but there is scant information on what constitutes an optimal serum 25-hydroxyvitamin D concentration to achieve this. In the study of Cheng et al. (5), girls with 25-hydroxyvitamin D concentrations < 25 nmol/L had lower cortical volumetric BMD of the distal radius and tibial shaft than girls with concentrations > 25 nmol/L. Another Finnish study of girls aged 14–16 y found serum concentrations < 40 nmol/L concomitant with low forearm BMD (7). Defining cutoff values for vitamin D insufficiency is further complicated by differences in values obtained by different 25-hydroxyvitamin D assays (38). Cognizant of the uncertainty of what defines vitamin D insufficiency, we chose a 25-hydroxyvitamin D value of 37.5 nmol/L as a cutoff value for vitamin D insufficiency.

Two large nationally representative surveys also reported serum 25-hydroxyvitamin D concentrations in children and adolescents; the NHANES III included data for adolescents 12–19 y (24) and the UK National Diet and Nutrition Survey (NDNS) included data on children 4–14 y (25). It would appear that the vitamin D status of UK children and adolescents is somewhat better, and of U.S. adolescents substantially better, than that of New Zealand children and adolescents. Data from NHANES III are confounded by latitude and season. Nevertheless, mean serum 25-hydroxyvitamin D in the winter in the American South (25–41°N) was 64.9 nmol/L in females and 78.6 nmol/L in males; <1% of 12–19 y olds had a serum 25-hydroxyvitamin D < 17.5 nmol/L and only 5 and 12% of males and females, respectively, had serum concentrations < 37.5 nmol/L. In NZ in the winter months (April-September), the mean serum 25-hydroxyvitamin D in children and adolescents 5–14 y was 43 nmol/L with 5 and 43% having vitamin D concentrations < 17.5 and < 37.5 nmol/L, respectively. In the UK NDNS, the mean serum 25-hydroxyvitamin D for children aged 4–10 y was 70 nmol/L and for ages 11–14 y the mean was 56 nmol/L. Almost no British children were defined as vitamin D deficient, based on a cutoff value of <12 nmol/L. The prevalence of insufficiency was lower than in NZ children; 8–15% of UK children aged 4–10 y were vitamin D insufficient (<40 nmol/L). In the 11–14 y age group, UK and NZ boys were similar but 30% of UK girls were vitamin D insufficient (<40 nmol/L) (25), compared with 43% of NZ girls aged 11–14 y having concentrations < 37.5 nmol/L. The better vitamin D status of British and U.S. than New Zealand children probably reflects higher consumption of vitamin D–fortified foods such as fortified milks and breakfast cereals, which are readily available in the U.S. and UK but not in New Zealand.

The 2 strongest determinants of serum 25-hydroxyvitamin D concentrations in New Zealand children were season and ethnicity. The decline of 25-hydroxyvitamin D concentrations by 30 nmol/L (a 50% decline) between March and August is typical of differences reported in regions of similar or higher latitude (39–41). Because the survey had no blood samples collected during January and February, our results may underestimate the true mean serum 25-hydroxyvitamin D status. In the National Nutrition Survey of New Zealand adults, the mean serum 25-hydroxyvitamin D concentration in January and February was 81 and 70 nmol/L, respectively, with a population mean of 50 nmol/L for the whole year (42). Assuming that the concentrations in children during January and February are the same as in adults, we estimate the mean serum 25-hydroxyvitamin D concentration for the whole year to be 54 nmol/L, only slightly higher than the survey result of 50 nmol/L.

Ethnicity had the next greatest effect on vitamin D status, with an adjusted mean difference of 16 nmol/L in serum 25-hydroxyvitamin D between Pacific and NZEO children. Pacific children had twice the risk of vitamin D insufficiency compared with NZEO children. There is a large variability in skin color within each of the 3 ethnic groups, particularly Mori and Pacific children. However, overall differences in average skin color among the 3 ethnic groups likely account for the ethnic differences in vitamin D status. The health implications of lower vitamin D status in Mori and Pacific children are not known. Paradoxically, Pacific adults in New Zealand have lower serum 25-hydroxyvitamin D concentrations (42,43), yet higher bone mineral content (44), BMD (45), and lower fracture rates (46) than European New Zealanders. To date, there are no data associating vitamin D status with chronic diseases in Mori or Pacific Peoples.

Obesity and sex each had an independent effect on serum vitamin D concentrations, although of lesser magnitude than season or ethnicity. Results from the CNS02 showed that physical inactivity increased considerably across age categories, was higher in girls than boys (26), and was higher in children who were obese rather than "normal" weight (unpublished findings). It is possible that sex and obesity are acting as surrogate markers for sunlight exposure through their association with physical activity. In the case of obesity, there is also evidence that serum 25-hydroxyvitamin D may be sequestered in adipose tissue (15). There was no effect of latitude on serum 25-hydroxyvitamin D. Only 174 participants were recruited from the South Island, and it may be that there was insufficient power to detect a difference in 25-hydroxyvitamin D concentrations across the narrow range of latitude (32–44°S).

Of the children who participated in the CNS02, 16% were from schools classified as rural and were not asked to provide a blood sample. The greater proportion of Pacific and North Island (89 vs. 84%) children likely reflects the exclusion of rural participants, who were more likely to be NZEO and live in the South Island. Differences in proportions of children who gave blood compared with those in the larger survey (Table 1) were accounted for by applying appropriate weights in the statistical analysis.

Using a cutoff value of 537.5 nmol/L for 25-hydroxyvitamin D concentration, we report a high prevalence of insufficient vitamin D status in New Zealand school-age children, from 31% for all children to a high of 59% in Pacific children. Unfortunately, there is little direct evidence to indicate that vitamin D concentrations at this level in children cause poor skeletal health or lead to a lower attainment of peak bone mass and higher rates of osteoporosis in older age. Moreover, the epidemiologic evidence linking low vitamin D status with increased risk of diabetes or some types of cancer is not yet of sufficient quality or strength to be convincing. The results of this survey warrant an urgent evaluation of what health risks may be experienced by New Zealand children with respect to their current vitamin D status.

	FOOTNOTES

 
¹ Presented in part at the Nutrition Society of Australia 28th Annual Scientific Meeting in conjunction with the Nutrition Society of New Zealand and the International Congress of Clinical Nutrition August, 2004, Brisbane, Australia [Green, T. J., Skeaff, C. M., Rockell, J. E., Taylor, R. W. & Whiting, S. J. (2004) Serum 25-hydroxyvitamin D status of New Zealand children. Asia. Pac. J. Nutr. 13 (suppl.): S46].

² A University of Otago Research Grant funded the vitamin D analysis. The 2002 Children’s Nutrition Survey was funded by the New Zealand Ministry of Health.

⁴ Abbreviations used: BMD, bone mineral density; CNS02, 2002 National Children’s Nutrition Survey; NHANES, National Health and Nutrition Examination Survey; NZEO, New Zealand European and Others; PTH, parathyroid hormone.

Manuscript received 17 May 2005. Initial review completed 12 July 2005. Revision accepted 15 August 2005.

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