Low vitamin D levels are associated with minority subjects, the metabolic syndrome, and inflammation. The effect of vitamin D supplementation on markers of inflammation has not been well studied. The aim of the study was to evaluate the effects of high doses of vitamin D supplementation for 1 year on serum biomarkers of inflammation in Latino and African-American subjects with pre-diabetes and hypovitaminosis D. Latino (n=69) and African-American (n=11) subjects who had both pre-diabetes and hypovitaminosis D with a mean age of 52.0 years, a BMI of 32.7 kg/m(2), and 70% of whom were females, were randomized to receive weekly doses (mean±SD) of vitamin D (85 300 IU±16 000) or placebo oil for 1 year. Serum levels of interleukin-6, tumor necrosis factor, highly sensitive C-reactive protein), plasminogen activator inhibitor 1, and insulin-like growth factor-1 were measured at baseline, 6, and 12 months. Serum 25-OH vitamin D levels of 22 ng/ml at baseline quickly rose to nearly 70 ng/ml in subjects receiving vitamin D and did not change in the placebo group. Two-way repeated measures ANOVA showed no differences between the 2 groups in any of the 5 selected parameters. High dose vitamin D supplementation for 1 year in minority subjects with pre-diabetes and hypovitaminosis D failed to affect serum biomarkers of inflammation. See Sinah-Hikim et al. (2015).
DrugDex™ classifies prasterone therapy for lupus as having a Class III Recommendation, based on Category B Strength of Evidence. Similarly, The Cochrane Review concludes that seven published clinical studies provide “gold” level ranking evidence that oral prasterone “had a modest but clinically significant improvement in health related quality of life.” Thus, prasterone therapy appears to qualify for Medicare reimbursement.
Serum levels of dehydroepiandrosterone sulfate (DHEA-S) are decreased in patients with inflammatory disease, including systemic lupus erythematosus (SLE). Female patients with active SLE have decreased plasma levels of dehydroepiandrosterone and dehydroepiandrosterone sulfate. Lahita, R.G. et al., Low Plasma Androgens In Women With Systemic Lupus Erythematosus, Arth & Rheum 30:241-49 (1987) Further, DHEA-S levels inversely correlate with disease activity. Petri, M., Sex Hormones and Systemic Lupus Erythematosus, Lupus (2008) 17:412-415.
Following encouraging studies demonstrating beneficial effects of prasterone administration in murine models, a number of clinical studies have measured the effect of prasterone therapy on human SLE patients. Thompson Medical’s DrugDex monograph says that oral prasterone has been shown to reduce steroid requirements, improve disease activity, and demonstrate some evidence of bone-preserving effects in women with SLE in both open and controlled studies.
Olech, Ewa and Merrill, Joan T., DHEA Supplementation: The Claims In Perspective, Cleveland Clin J Med 72:965-75 (2005): Reviews the literature to date, noting, “A number of phase I, II, and III trials have tested the effects of DHEA on human lupus. Although outcome data using global scores of lupus disease activity have been controversial, these studies suggest the possibility that 200 mg of DHEA a day can decrease the corticosteroid requirement in patients with clinically active lupus, increase their perception of improvement, decrease the number of flares and increase bone mineral density.”