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High-dose vitamin D supplements act as anti-inflammatory

By Stephen Daniells , 10-Apr-2006

A high-dose vitamin D supplement inhibit pro-inflammatory and boost anti-inflammatory molecules and could help people with heart failure, says a German clinical trial.

"We showed for the first time that a daily supplement of 50 micrograms vitamin D for nine months is able to increase serum concentrations of the anti-inflammatory cytokine IL-10 and to prevent an increase in serum concentrations of the pro-inflammatory cytokine TNF-alpha in CHF patients," wrote lead author Stefanie Schleithoff from the University of Bonn.

According to the Study on Heart failure Awareness and Perception in Europe (SHAPE), about 14m people in Europe suffer from chronic heart failure (CHF) with the number forecast to rise to 30 m by 2020. About 5m people suffer from the condition in the US.

The cause of CHF is not understood, but recent theories involve increased levels of pro-inflammatory cytokines, such as tumour necrosis factor alpha (TNF-alpha).

The randomised placebo-controlled trial, published in the April issue of the American Journal of Clinical Nutrition (Vol. 83, pp. 754-759), followed the effects of a high-dose vitamin D3 supplement (50 micrograms, equivalent to 2000 International Units) on cytokine levels and heart pumping ability of 123 patients with CHF.

Both placebo and vitamin D supplement groups were also given a daily supplement of 500 milligrams of calcium.

After nine months the researchers reported that serum levels of 25-hydroxyvitamin D, the non-active 'storage' form of the vitamin in the body, increased by 26.8 nanograms per millilitre (ng/mL) from the start of the study for the supplemented group, while the placebo group's levels decreased by 3.6 ng/mL, a not-too-unexpected result.

Levels of TNF-alpha did not differ significantly before or after supplementation with vitamin D, but it did increase by 12 per cent in the placebo group. Interleukin 10 (IL-10) levels increased by an impressive 43 per cent in the supplemented group, but did not change in the placebo group.

No significant difference was observed in heart function, as measured by left ventricular ejection fraction (LVEF), for either of the groups; a result that differs from a previous study with lower vitamin D doses (400 IU) that reported improvements in LVEF, but no improvement in cytokine levels.

Twenty-five patients dropped out of the trial because of a worsening in health. However, the authors point out that these patients all had markedly higher levels of many pro-inflammatory markers at the start of the trial.

In an accompanying editorial by Reinhold Vieth and Samantha Kimball from the University of Toronto, said that the study offered two important insights: "First, the article confirms previous evidence that vitamin D supplementation affects immune-modulating cytokines in desirable ways. Second, it points to a higher dose requirement for achieving this."

Vitamin D has been reported to improve muscular function, control blood pressure, and improve glucose tolerance, all of which underlying causes of CHF, said Vieth and Kimball.

"The more realistic question raised by Schleithoff et al is whether the use of an appropriate dose of vitamin D, as one part of a nutritional strategy, could help in the primary prevention of CHF," concluded the editorial.

The results of this clinical trial appear to be in line with a study published in the Journal of the American College of Cardiology (2003, Vol. 41, pp. 105-112) which reported that heart disease was linked to vitamin D deficiency.

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