Atherosclerosis, Thrombosis, and Vascular Biology – Sept 2012 (American Heart Association)
Manish P. Ponda, Kathleen Dowd, Dennis Finkielstein, Peter R. Holt, Jan L. Breslow
From the Laboratory of Biochemical Genetics and Metabolism (M.P.P., P.R.H., J.L.B.) and the Center for Clinical and Translational Science (K.D.), The Rockefeller University, New York, NY; and Beth Israel Medical Center, New York, NY (D.F.).
Correspondence to Jan L. Breslow, Laboratory of Biochemical Genetics and Metabolism, The Rockefeller University, Box 179, New York, NY 10065. E-mail breslow at rockefeller.edu
Objective—Vitamin D deficiency is common and associated with dyslipidemia. However, it is unclear whether oral vitamin D supplementation improves the lipid profile. Therefore, we conducted a randomized, placebo-controlled trial to determine the short-term effects of vitamin D repletion on the lipid profile.
Methods and Results—One hundred fifty-one vitamin D?deficient (25-hydroxyvitamin D <20 ng/mL) adults with elevated risk for cardiovascular disease were randomized to receive either 50 000 IU of vitamin D3 weekly for 8 weeks or placebo. The primary outcome was the change in small low-density lipoprotein (LDL) particle number. Secondary outcomes included changes in other nuclear magnetic resonance?based and chemical lipid fractions. Vitamin D failed to improve the lipid profile.
Compared with the placebo, vitamin D repletion did not change small LDL particle number (mean change, +18 nmol/L; 95% CI [?80 to +116 nmol/L]; P=0.63). There were also no changes in the chemical lipid profile: total cholesterol (+5.8 mg/dL, 95% CI [?1.4 to +13.0 mg/dL], P=0.14); LDL cholesterol (+3.8 mg/dL, 95% CI [?2.5 to +10.2 mg/dL], P=0.13); high–density lipoprotein cholesterol (+0.4 mg/dL 95% CI [?1.6 to +2.6 mg/dL], P=0.71); and triglycerides (+7.9 mg/dL 95% CI [?6.5 to +22.3 mg/dL]). In the vitamin D repletion group, exploratory multivariate regression analysis demonstrates that changes in LDL cholesterol were positively correlated with the changes in serum calcium (P<0.001) and inversely with the changes in serum parathyroid hormone (P=0.02).
Conclusion—In contrast to the association between low 25-hydroxyvitamin D levels and dyslipidemia, correcting vitamin D deficiency in the short-term does not improve the lipid profile. Repletion of 25-hydroxyvitamin D levels raised serum calcium levels and decreased serum parathyroid hormone levels. These expected physiological responses to vitamin D therapy were correlated with a significant increase in LDL cholesterol.
8 weeks is just about enough time to replete the vitamin D levels for healthy, normal weight persons.
If the RCT had lasted 12-16 weeks then the cholesterol levels probably would have gone down.
It is strange that the abstract did not mention the vitamin D levels before and after the RCT.
What did they consider to be repletion: 20 ng, 30 ng, or what?
The clinical trial indicates that only people with < 20 ng of vitamin D were accepted.
The clinical trial also indicates that the people should have BMI > 35 kg/m2
- which is enough weight that it takes more than 8 weeks time to replete vitamin D without loading doses.
50,000 IU of vitamin D (7,000 IU daily) should not be used as a monotherapy - cofactors should be adjusted if > 4,000 IU