Ignite Creation Date:
2024-05-05 @ 10:12 PM
Last Modification Date:
2024-10-26 @ 10:15 AM
Study NCT ID:
NCT01050387
Status:
COMPLETED
Last Update Posted:
2014-08-05
First Post:
2010-01-13
Brief Title:
Effects of Vitamin D Dose and Genotype of the Binding Protein in Infants and Children
Sponsor:
Yale University
Organization:
Yale University
Study Overview
Official Title:
A Randomized Controlled Trial of Vitamin D Supplementation in Infants and Children Effects of Vitamin D Dose and Genotype of the Binding Protein
Status:
COMPLETED
Status Verified Date:
2013-07
Last Known Status:
None
Delayed Posting:
No
If Stopped, Why?:
Not Stopped
Has Expanded Access:
False
If Expanded Access, NCT#:
N/A
Has Expanded Access, NCT# Status:
N/A
Acronym:
VitaD
Brief Summary:
The purpose of this study is to determine if the vitamin D binding protein genotype influences circulating vitamin D levels and if it may have functional consequences on vitamin D activity
Detailed Description:
Vitamin D has recently been the subject of much attention Advantages to the prevention of vitamin D deficiency VDD in young children are obvious acutely hypocalcemic seizures may occur in VDD and rickets can result in long-term skeletal deformities Previous research has emphasized the importance of identifying optimal supplementation doses and appropriate target thresholds for circulating 25-hydroxyvitamin D 25-OHD the best described marker of vitamin D status The timely next step is to objectively establish effective doses for the prevention of VDD without creating risk from overzealous supplementation in a population representative of those most at risk for overt disease
Although the primary role of vitamin D is considered to be its effect on intestinal calcium absorption enormous variability of fractional calcium absorption in relation to 25-OHD levels exists We provide evidence that a significant component of this variability is genetic in nature and in particular relates to vitamin D binding protein DBP genotype
The aggregate data suggest that the critical mechanism for the development of nutritional rickets is reduction in availability of calcium to the skeleton which is largely determined by vitamin D status and intestinal calcium absorption Our proposal focuses on the establishment of a workable definition of vitamin D deficiency in an underserved and highly vulnerable population and to assess the impact of genetic variance in VDR and DBP as factors to be considered in the recommendation of vitamin D status assessment taking into account the outcome of 25-OHD level and in additional studies potential functional consequences of vitamin D related to both its classical and non-classical effects
Although the primary role of vitamin D is considered to be its effect on intestinal calcium absorption enormous variability of fractional calcium absorption in relation to 25-OHD levels exists We provide evidence that a significant component of this variability is genetic in nature and in particular relates to vitamin D binding protein DBP genotype
The aggregate data suggest that the critical mechanism for the development of nutritional rickets is reduction in availability of calcium to the skeleton which is largely determined by vitamin D status and intestinal calcium absorption Our proposal focuses on the establishment of a workable definition of vitamin D deficiency in an underserved and highly vulnerable population and to assess the impact of genetic variance in VDR and DBP as factors to be considered in the recommendation of vitamin D status assessment taking into account the outcome of 25-OHD level and in additional studies potential functional consequences of vitamin D related to both its classical and non-classical effects
Study Oversight
Has Oversight DMC:
None
Is a FDA Regulated Drug?:
None
Is a FDA Regulated Device?:
None
Is an Unapproved Device?:
None
Is a PPSD?:
None
Is a US Export?:
None
Is an FDA AA801 Violation?:
None
Secondary IDs
| Secondary ID | Type | Domain | Link |
|---|---|---|---|
| M136410 | US NIH GrantContract | None | httpsreporternihgovquickSearch1RC1HD063562 |
| 1RC1HD063562 | NIH | None | None |