Am J Clin Nutr. 2006 Apr;83(4):754-9.Schleithoff SS1, Zittermann A, Tenderich G, Berthold HK, Stehle P, Koerfer R.Author information1Institute of Nutrition and Food Science, University of Bonn, Bonn, Germany.AbstractBACKGROUND: Elevated circulating concentrations of proinflammatory cytokines may contribute to the pathogenesis of congestive heart failure (CHF). In vitro studies suggest that vitamin D suppresses proinflammatory cytokines and increases antiinflammatory cytokines.OBJECTIVE: We evaluated the effect of vitamin D supplementation on the survival rate and different biochemical variables in patients with CHF.DESIGN: One hundred twenty-three patients randomly received either 50 mug vitamin D(3)/d plus 500 mg Ca/d [D(+) group] or placebo plus 500 mg Ca/d [D(-) group] for 9 mo. Biochemical variables were assessed at baseline and after 9 mo. The survival rate was calculated for a follow-up period of 15 mo.RESULTS: Ninety-three patients completed the study. Significant treatment effects were observed on logarithmic-transformed serum concentrations of 25-hydroxyvitamin D (P = 0.001), parathyroid hormone (P = 0.007), tumor necrosis factor alpha (P = 0.006), and interleukin 10 (P = 0.042).
25-Hydroxyvitamin D increased by 26.8 ng/mL in the D(+) group but increased only by 3.6 ng/mL in the D(-) group. Compared with baseline, parathyroid hormone was significantly lower and the antiinflammatory cytokine interleukin 10 was significantly higher in the D(+) group after 9 mo. The proinflammatory cytokine tumor necrosis factor alpha increased in the D(-) group but remained constant in the D(+) group. The survival rate did not differ significantly between the study groups during the follow-up period.CONCLUSIONS: Vitamin D(3) reduces the inflammatory milieu in CHF patients and might serve as a new antiinflammatory agent for the future treatment of the disease. Our data provide evidence for the involvement of an impaired vitamin D-parathyroid hormone axis in the progression of CHF.PMID: 16600924 [Indexed for MEDLINE] Publication typesRandomized Controlled TrialResearch Support, Non-U.S. Gov'tMeSH termsChronic DiseaseDietary SupplementsDisease ProgressionDouble-Blind MethodFemaleHeart Failure/blood*Heart Failure/mortalityHeart Failure/physiopathologyHumansInterleukin-10/biosynthesisInterleukin-10/blood*MaleMiddle AgedParathyroid Hormone/blood*Survival RateTumor Necrosis Factor-alpha/metabolism*Vitamin D/administration & dosage*Vitamin D/analogs & derivatives*Vitamin D/bloodVitamins/administration & dosage*Vitamins/bloodSubstancesParathyroid HormoneTumor Necrosis Factor-alphaVitaminsInterleukin-10Vitamin D25-hydroxyvitamin DFull Text SourcesHighWireOther Literature SourcesCited by Patents in - The LensMedicalClinicalTrials.govHeart Failure - MedlinePlus Health InformationVitamin D - MedlinePlus Health Information
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Load citing article information Articles by O’Connor, L. E. Articles by Campbell, W. W. Obesity and Metabolism Research ArticlesAbstractAn estimated 1 billion people worldwide have deficient or insufficient levels of vitamin D. Even more alarming is the association of vitamin D deficiency with many types of diseases, particularly heart failure (HF). Hypovitaminosis D has been observed to be highly prevalent in the HF community with rates varying from approximately 80% to 95%. Higher rates of deficiency have been linked to winter months, in patients with protracted decompensated HF, darker skin pigmentation, and higher New York Heart Association (NYHA) classes. In fact, some data suggest vitamin D deficiency may even be an independent predictor of mortality in patients with HF. Traditionally obtained through UV exposure and activated in the liver and then the kidneys, vitamin D is classified as a vitamin but functions as a steroid hormone. The hormone acts through the vitamin D receptor (VDR), which is expressed in vascular smooth muscle cells, renal juxtaglomerular cells, and most interestingly, cardiac myocytes.
Studies have shown that the association between vitamin D deficiency and HF often manifests in the structural components of cardiac myocytes and/or through alterations of the neurohormonal cascade. In addition, vitamin D may also act rapidly through intracellular nongenomic receptors that alter cardiac contractility. Unfortunately, prospective vitamin D supplementation trials show mixed results. In rat models, successful correction of deficiency was associated with reductions in ventricular hypertrophy. In humans, however, echocardiographic dimensions did not change significantly. These results bring into questions whether vitamin D is a risk factor for HF, a marker of HF disease severity, or has a true pathologic role. This article provides a thorough review of vitamin D deficiency etiology, prevalence, and possible pathophysiologic role in HF. Furthermore, we carefully review prospective trials on vitamin D therapy in HF. We believe more trials on vitamin D therapy in HF need to be conducted before any conclusions can be drawn.