Clinical and biomarker modifiers of vitamin D treatment response: the Multi-Ethnic Study of Atherosclerosis.

Dec 1, 2021The American journal of clinical nutrition

Factors that may change how people respond to vitamin D treatment.

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Abstract

Among 666 older adults, lower baseline 25-hydroxyvitamin D levels were linked to a greater decline in parathyroid hormone levels with vitamin D3 supplementation.

Participants receiving vitamin D3 experienced a mean decrease in parathyroid hormone of -3 pg/mL, while those on placebo had an increase of 2 pg/mL.
A significant difference in parathyroid hormone reduction was observed in participants with baseline 25-hydroxyvitamin D levels below 20 ng/mL, showing a decline of -10 pg/mL.
No significant change in 1,25-dihydroxyvitamin D levels was noted in either treatment group.
Race/ethnicity, BMI, and estimated glomerular filtration rate did not affect the response to vitamin D supplementation.
A baseline 25-hydroxyvitamin D concentration of 21 ng/mL was identified as a threshold for changes in parathyroid hormone levels.

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BACKGROUND: Different 25-hydroxyvitamin D [25(OH)D] thresholds for treatment with vitamin D supplementation have been suggested and are derived almost exclusively from observational studies. Whether other characteristics, including race/ethnicity, BMI, and estimated glomerular filtration rate (eGFR), should also influence the threshold for treatment is unknown.

OBJECTIVES: The aim was to identify clinical and biomarker characteristics that modify the response to vitamin D supplementation.

METHODS: A total of 666 older adults in the Multi-Ethnic Study of Atherosclerosis (MESA) were randomly assigned to 16 wk of oral vitamin D3 (2000 IU/d; n = 499) or placebo (n = 167). Primary outcomes were changes in serum parathyroid hormone (PTH) and 1,25-dihydroxyvitamin D [1,25(OH)2D] concentrations from baseline to 16 wk.

RESULTS: Among 666 participants randomly assigned (mean age: 72 y; 53% female; 66% racial/ethnic minority), 611 (92%) completed the study. The mean (SD) change in PTH was -3 (16) pg/mL with vitamin D3 compared with 2 (18) pg/mL with placebo (estimated mean difference: -5; 95% CI: -8, -2 pg/mL). Within the vitamin D3 group, lower baseline 25-hydroxyvitamin D [25(OH)D] was associated with a larger decline in PTH in a nonlinear fashion. With baseline 25(OH)D ≥30 ng/mL as the reference, 25(OH)D <20 ng/mL was associated with a larger decline in PTH with vitamin D3 supplementation (-10; 95% CI: -15, -6 pg/mL), whereas 25(OH)D of 20-30 ng/mL was not (-2; 95% CI: -6, 1 pg/mL). A segmented threshold model identified a baseline 25(OH)D concentration of 21 (95% CI: 13, 31) ng/mL as an inflection point for difference in change in PTH. Race/ethnicity, BMI, and eGFR did not modify vitamin D treatment response. There was no significant change in 1,25(OH)2D in either treatment group.

CONCLUSIONS: Of characteristics most commonly associated with vitamin D metabolism, only baseline 25(OH)D <20 ng/mL modified the PTH response to vitamin D supplementation, providing support from a clinical trial to use this threshold to define insufficiency. This trial was registered at clinicaltrials.gov as NCT02925195.

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