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AREDS2 provides answers – and more questions
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While it is true that history is made in eye care on a daily basis, it is only on rare occasions we witness an event of epic proportion – something that forever alters the way we think about a particular aspect of clinical practice. Such paradigm shifts are oft times the result of a landmark study. Recently we witnessed such an event with the completion of the Age-Related Eye Disease Study 2 (AREDS2).
Since its inception in 2006, the conclusions derived from AREDS2 have been greatly anticipated. After all, AREDS2 is the heir apparent to AREDS, itself a seminal study that forever changed the way clinicians view nutrition and age-related macular degeneration. While the magnitude of AREDS provided us with irrefutable results, it also yielded numerous subanalyses … and as many questions as it did answers.
Will the AREDS formula without beta carotene be effective? Do lutein and zeaxanthin play a role in mitigating the progression of AMD? This is perhaps the most highly anticipated question: Are omega-3s beneficial in slowing the progression of AMD?
Indeed, since its inception in 2006, researchers, clinicians, industry and the public have anxiously awaited answers to these questions. As the AREDS2 results were unveiled earlier this year at the Association for Research in Vision and Ophthalmology meeting and subsequently in JAMA, they have been met with mixed emotions.
We were thrilled to see lutein/zeaxanthin replace beta carotene, providing a safe and effective formulation for smokers and nonsmokers alike. We were also pleased to see the safety of zinc, at 80 mg, vindicated. However, the lack of discernible benefit in adding omega-3s to the mix was a bit of a disappointment for many. After all, how could EPA and DHA – highly regarded across so many medical disciplines – fail to benefit our patients with AMD? More importantly, how does this news impact the way we recommend omega-3s to our patients?
It is implicit we applaud, respect and embrace the efforts of everyone involved in AREDS2. The results of this study must be reflected in how we counsel and treat patients. However, with respect to the role of omega-3s in AMD, it might well be that AREDS2 has raised more questions than provided answers.
Were the amounts of EPA and DHA optimal for mitigating AMD progression? Could the fact that AREDS2 subjects were better nourished than the population at large have actually masked the true benefits of EPA and DHA? Perhaps most importantly, are EPA and DHA more important in prophylaxis – rather than treatment – of AMD?
This is not meant to be critical of AREDS2 in any way, as none of these questions were primary endpoints of the study. However, they underscore the importance of interpreting, before adapting, study results into clinical practice.
So, where do we go from here? If you have not already done so, read the AREDS2 report … in its entirety. Digest it, incorporate it and share it with applicable patients in a meaningful way. But, above all, keep an open mind, as it is just a matter of time before history is made … again.