Kumaravel Rajakumar

Vitamin D Status, Adiposity, and Lipids in Black American and Caucasian Children

OBJECTIVE The aim of the study was to examine the relationship between vitamin D status, total and abdominal adiposity, and lipids in black and white children. METHODS Plasma 25-hydroxyvitamin D [25(OH)D], adiposity [body mass index (BMI), percentage of total body fat, visceral adipose tissue (VAT), sc adipose tissue (SAT)], and fasting lipids were assessed in healthy obese and nonobese 8- to 18-yr-old black and white children. RESULTS We studied 237 children (mean ± sd age, 12.7 ± 2.2 yr; 47% black, 47% obese, and 43% male). Mean 25(OH)D concentration for the entire cohort was 19.4 ± 7.4 ng/ml. The majority of the children were vitamin D deficient [25(OH)D < 20 ng/ml; 73% blacks, 40% whites]. Plasma 25(OH)D was associated inversely with BMI, BMI percentile, percentage of total body fat, VAT, and SAT and positively with HDL cholesterol in the entire cohort. VAT was higher in vitamin D-deficient whites, and SAT was higher in vitamin D-deficient blacks compared with their respective vitamin D-nondeficient counterparts. Race, season, pubertal status, and VAT were independent significant predictors of 25(OH)D status. CONCLUSIONS In black and white youth examined together, lower levels of 25(OH)D are associated with higher adiposity measures and lower HDL. Furthermore, vitamin D deficiency is associated with higher VAT in whites and greater SAT in blacks. Besides therapeutic interventions to correct the high rates of vitamin D deficiency in youth, benefits of vitamin D optimization on adiposity measures and lipid profile need to be explored.

Vitamin D Status and Response to Vitamin D3 in Obese vs. Non-obese African American Children

Background: Serum 25‐hydroxyvitamin D (25(OH)D) is low in obese adults.

SOLAR Ultraviolet Radiation AND Vitamin D

Rickets, the state of vitamin D deficiency, has reemerged as a potential problem in the United States. At the dawn of the 20th century, rickets was pervasive among infants residing in the polluted cities of Europe and the northeastern United States. Important milestones in the history of rickets were the understanding that photosynthesized vitamin D and dietary vitamin D were similar, the discernment of the antirachitic potency of artificial and natural ultraviolet rays, and the discovery that ultraviolet irradiation could render various foods antirachitic. Clinical guidelines were instituted to promote sensible exposure to sunlight and artificial ultraviolet radiation. In addition, irradiated ergosterol from yeast became the major vitamin D source for food fortification and the treatment of rickets, leading to a public health campaign to eradicate rickets by the 1930s. We review the sequence and turn of events pertaining to the discovery of vitamin D and the strategies for the eradication of the reemerging rickets problem.

Vitamin D Insufficiency in Preadolescent African-American Children

To determine the proportion of vitamin D insufficiency in 6- to 10-year-old preadolescent African-American children residing in Pittsburgh, Pennsylvania and to estimate their therapeutic response to vitamin D 400 IU/day for 1-month, an open-label pre- and post-comparison of vitamin D status following vitamin D 400 IU daily for 1 month during winter and early spring was conducted. Outcomes included serum calcium, phosphorus, albumin, 25 hydroxyvitamin D [25 (OH) D], 1, 25 dihydroxyvitamin D [1, 25 (OH) 2 D], parathyroid hormone (PTH), and markers of bone turnover (serum bone-specific alkaline phosphatase, osteocalcin, and urine n-telopeptide crosslinked collagen type 1 [NTX]). Dietary intake of vitamin D was assessed using a food frequency questionnaire. Forty-one of the 42 enrolled subjects (mean age: 8.9 ± 1.2 yrs [SD]) were analyzed, and 20/41 (49%) were vitamin D insufficient. Vitamin D insufficient group had a suggestive trend of being older (9.2 ± 1.0 years vs. 8.5 ± 1.3 years, p = 0.06) and more pubertally advanced (Tanner II: 7/20 vs. Tanner II: 1/21, p = 0.02). Mean dietary intake of vitamin D was 277 (146 IU/day (n = 41). Adequate intake for vitamin D (200 IU/day) was not met in 16/41 (39%); however, the dietary intake of vitamin D was not significantly different between the vitamin D insufficient and vitamin D sufficient groups.

Racial Differences in Parents' Distrust of Medicine and Research

OBJECTIVE To assess and compare the attitudes and trust that African American and white parents have toward their children participating in research. DESIGN Self-administered, cross-sectional survey of a convenience sample of parents. SETTING Primary Care Center at Childrens Hospital of Pittsburgh from August 2004 through April 2005. PARTICIPANTS One hundred ninety parents (140 African American and 50 white parents). OUTCOME MEASURE Parental distrust of medical research as measured by a summative score of distrusting responses to 8 questions assessing trust in research. RESULTS African American parents had significantly greater distrust than white parents (67% vs 50%, P = .04). Education was also associated with having significantly greater distrust (74% of those with <high school education vs 44% of college graduates, P = .03). However, African American race remained a predictor of distrust even when education was controlled for (odds ratio, 2.25; 95% confidence interval, 1.01-5.01). CONCLUSIONS The degree of parental distrust toward medical research was significantly greater among African American parents. Parental distrust may be a barrier to enrollment of African American children in clinical research. Strategies for overcoming the higher level of distrust in African American parents are warranted for ensuring adequate representation of African American children in clinical research.

Impact of Season and Diet on Vitamin D Status of African American and Caucasian Children

Seasonal variation of vitamin D status and adequacy of dietary vitamin D and impact of race on maintaining vitamin D sufficiency was assessed in 140 healthy 6- to 12-year-old African American (AA) and Caucasian (C) children residing in Pittsburgh, Pennsylvania during summer and winter. Vitamin D insufficiency was not rare in either group (AA vs C, summer, 17.2% vs 14.3%, nonsignificant; winter, 34.1% vs 32.5%, nonsignificant) despite a mean dietary intake of vitamin D above the American Academy of Pediatrics (AAP) recommended intake (400 IU/d; AA vs C, summer, 421 vs 456 IU/d, nonsignificant; winter, 507 vs 432 IU/d, nonsignificant). Race/season and dietary vitamin D were predictors of serum 25-hydroxyvitamin D [25(OH)D] concentrations. However, dietary vitamin D influenced 25(OH)D only in Caucasians during winter. Current AAP recommended daily intake for vitamin D is inadequate for maintaining vitamin D sufficiency in children.

25-Hydroxyvitamin D Concentrations and In Vivo Insulin Sensitivity and β-Cell Function Relative to Insulin Sensitivity in Black and White Youth

OBJECTIVE To examine the relationships between plasma 25-hydroxyvitamin D [25(OH)D] and in vivo insulin sensitivity and β-cell function relative to insulin sensitivity, disposition index (DI), in black and white youth. RESEARCH DESIGN AND METHODS Plasma 25(OH)D concentrations were analyzed in banked specimens in healthy youth aged 8 to 18 years who had existing data on hyperinsulinemic-euglycemic and hyperglycemic clamp to assess insulin sensitivity and secretion, and measurements of body composition, and abdominal visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT). RESULTS A total of 183 research volunteers (mean ± SD; age, 12.6 ± 2.2 years; 98 white, 98 male, 92 obese) were studied. Analysis of HbA1c, fasting glucose and insulin, insulin sensitivity, and DI across quartiles of plasma 25(OH)D revealed no differences among whites. In blacks, the observed significance of higher insulin sensitivity and DI in the highest quartile of 25(OH)D disappeared after adjusting for any of the adiposity measures (BMI or fat mass or VAT or SAT). The difference in insulin sensitivity (9.4 ± 1.2 vs. 5.6 ± 0.5 mg/kg/min per μU/mL; P = 0.006) between 25(OH)D nondeficient (≥20 ng/mL) versus deficient (<20 ng/mL) black youth also was negated when adjusted for adiposity. CONCLUSIONS In healthy youth, plasma 25(OH)D concentrations bear no independent relationship to parameters of glucose homeostasis and in vivo insulin sensitivity and β-cell function relative to insulin sensitivity. It remains to be determined whether in youth with dysglycemia the relationships are different and whether vitamin D optimization enhances insulin sensitivity and β-cell function.

25-Hydroxyvitamin D in Obese Youth Across the Spectrum of Glucose Tolerance From Normal to Prediabetes to Type 2 Diabetes

OBJECTIVE To 1) determine if plasma 25-hydroxyvitamin D (25[OH]D) concentrations differ among obese youth with normal glucose tolerance (NGT) versus prediabetes versus type 2 diabetes and 2) assess the relationships between 25(OH)D and in vivo insulin sensitivity and β-cell function in this cohort. RESEARCH DESIGN AND METHODS Plasma 25(OH)D concentrations were examined in banked specimens in 9- to 20-year-old obese youth (n = 175; male 42.3%, black 46.3%) (NGT, n = 105; impaired glucose tolerance [IGT], n = 43; type 2 diabetes, n = 27) who had in vivo insulin sensitivity and secretion measured by hyperinsulinemic-euglycemic and hyperglycemic clamp techniques and had an assessment of total body composition and abdominal adiposity. RESULTS The mean age and BMI of the subjects were 14.3 ± 2.1 years and 35.7 ± 5.6 kg/m2, respectively. BMI, plasma 25(OH)D, and the proportion of vitamin D–deficient and –insufficient children did not differ across the three groups. Furthermore, there was no association between 25(OH)D and in vivo insulin sensitivity or β-cell function relative to insulin sensitivity (disposition index) in all groups combined or in each group separately. CONCLUSIONS Our data in obese youth show 1) no differences in plasma 25(OH)D concentrations across the glucose tolerance groups and 2) no relationship between 25(OH)D and in vivo insulin sensitivity and β-cell function relative to insulin sensitivity in any of the groups. It remains uncertain if enhancement of the vitamin D status could improve pathophysiological mechanisms of prediabetes and type 2 diabetes in obese youth.

Effect of Vitamin D3 Supplementation in Black and in White Children: A Randomized, Placebo-Controlled Trial

CONTEXT Dosages of vitamin D necessary to prevent or treat vitamin D deficiency in children remain to be clarified. OBJECTIVE To determine the effects of vitamin D3 1000 IU/d on serum 25-hydroxyvitamin D [25(OH)D], PTH, and markers of bone turnover (osteocalcin and collagen type 1 cross-linked C-telopeptide) in black children and white children, and to explore whether there is a threshold level of 25(OH)D associated with maximal suppression of serum PTH concentration. DESIGN Healthy 8- to 14-year-old Pittsburgh-area black (n = 84) and white (n = 73) children not receiving vitamin supplements, enrolled from October through March from 2008 through 2011, were randomized to vitamin D3 1000 IU or placebo daily for 6 months. RESULTS The mean baseline concentration of 25(OH)D was <20 ng/mL in both the vitamin D-supplemented group and the placebo group (19.8 ± 7.6 and 18.8 ± 6.9 ng/mL, respectively). The mean concentration was higher in the supplemented group than in the placebo group at 2 months (26.4 ± 8.1 vs 18.9 ± 8.1 ng/mL; P < .0001) and also at 6 months (26.7 ± 7.6 vs 22.4 ± 7.3; P = .003), after adjusting for baseline 25(OH)D, race, gender, pubertal status, dietary vitamin D intake, body mass index, and sunlight exposure. Increases were only significant in black children, when examined by race. The association between 25(OH)D and PTH concentrations was inverse and linear, without evidence of a plateau. Overall, vitamin D supplementation had no effect on PTH and bone turnover. CONCLUSIONS Vitamin D3 supplementation with 1000 IU/d in children with mean baseline 25(OH)D concentration <20 ng/mL effectively raised their mean 25(OH)D concentration to ≥20 ng/mL but failed to reach 30 ng/mL. Vitamin D supplementation had no effect on PTH concentrations.

Dosing Error With Over-the-Counter Vitamin D Supplement: A Risk for Vitamin D Toxicity in Infants

Vitamin D, the “sunshine vitamin,” is back in the limelight.1 Reemergence of rickets among vulnerable infants (dark-skinned and/or breast-fed without vitamin D supplementation) and reports of excessive prevalence of vitamin D deficiency and insufficiency among children have reemphasized the importance of optimal intakes of vitamin D.2–5 The American Academy of Pediatrics (AAP) increased its recommended dietary allowance (RDA) of vitamin D for the prevention of vitamin D deficiency in infants and children from 200 IU to 400 IU in 2008.6–7 Recently, the Institute of Medicine (IOM) revised its RDA for vitamin D from 200 IU to 400 IU in infants (0 to 12 months) and from 200 IU to 600 IU in children (1 to 8 years).8 Without fortification, very few foods are rich in vitamin D. Humans meet their vitamin D needs from sunlight exposure, diet and/or supplements. Of these sources, photosynthesized vitamin D is the major contributor to human vitamin D status.9–11 Vitamin D-fortified milk and infant formula remains the main dietary source of vitamin D. An infant or a child must drink 4 servings (1 liter or 32 ounces) of vitamin D-fortified milk to meet the AAP recommended intake of vitamin D (400 IU/day), which seems to be a tall order for many. Therefore, vitamin D supplements become an important source of dietary vitamin D. In order to meet consumer desires to prevent deficiencies or optimize health benefits related to vitamin D, preparations of higher concentrations of over-the-counter vitamin D supplements have become readily available for the general public, with the potential for inadvertent overdosing in young infants and children.