Selenium: Great Claims, Few Data

Summary and Comment |
February 16, 2007

Selenium: Great Claims, Few Data

  1. Abigail Zuger, MD

Selenium supplementation was associated with better virologic control in a small blinded study. Could effective antiretrovirals have had something to do with it?

  1. Abigail Zuger, MD

The trace mineral selenium has documented in vitro activity against HIV and has acquired a certain cachet as a particularly valuable micronutrient for HIV-infected people. However, although clinical deterioration in AIDS has been associated with selenium deficiency, no cause-and-effect relation has been established. Researchers sought to determine if selenium has any therapeutic value, either by itself or in addition to antiretroviral treatment.

In a blinded study, 262 Miami-area adults with HIV infection but no other major medical problems were randomized to take a selenium supplement (200 μg daily) or placebo for 18 months. None were selenium-deficient at outset. Participants were primarily black or Hispanic men and had a mean CD4 count >400 cells/mm3. More than 60% of participants had a diagnosis of AIDS, and 192 (73%) were taking antiretrovirals. About half of the antiretroviral-treated participants had detectable viral loads (even though mean self-reported adherence to antiretrovirals exceeded 95% in both selenium and placebo recipients). Participants were followed monthly for study-drug pill counts and serum selenium levels; CD4-cell counts and viral loads were repeated at 9 and 18 months.

Only the 9-month data were analyzed for this report, by which time 88 participants (34%) had been lost to follow-up. Overall, rise in serum selenium level correlated with a fall in viral load and a rise in CD4-cell count. Within the selenium group, only 50 participants (54%) had a significant rise in serum selenium levels. These individuals had far better adherence to the experimental medicine (as measured by electronic monitoring caps) than did the other selenium recipients. At 9 months, their viral loads were not significantly changed from baseline, and their CD4-cell counts had risen significantly. In contrast, the other selenium recipients were essentially indistinguishable from placebo recipients, with unchanged serum selenium levels, higher viral loads than at baseline, and lower CD4-cell counts.

These results remained consistent after adjustment for a variety of social and medical cofactors. However, the high percentage of subjects with virologic failure suggests that self-reports of adherence to antiretroviral therapy at baseline were not entirely accurate. No objective measure of ongoing antiretroviral adherence was built into the study, and researchers did not make note of any changes in antiretroviral regimens.


The authors claim to show that daily selenium supplementation can lower viral load and indirectly raise CD4-cell counts. An alternative interpretation of the data, however, is that individuals who were adherent to the selenium were also adherent to their antiretrovirals and, in addition, were more likely to have had failing antiretroviral regimens changed by their primary providers during the course of the study. Without more detail regarding the background antiretrovirals in this study, no firm conclusions can be drawn. Perhaps such information will be forthcoming in a publication detailing the 18-month data. In the meantime, selenium use, whether alone or in addition to antiretroviral therapy, must still be considered an unproven intervention.


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