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There have been two papers published recently which, at first glance, may appear somewhat contradictory but both have significant implications. It is important for all eye care practitioners to be able to give appropriate advice about common eye diseases.
An up-to-date knowledge of risk factors is not only one of the GOC core competency requirements, but also an essential way for us to keep our patients properly informed about things they can do to help in the fight against long-term eye disease.
As age-related macular degeneration affects a major proportion of our patients, it is in this area that much interest has been focused in recent years. There are many risk factors for AMD, some non-modifiable (age, genetic make up, ethnicity and so on) and some modifiable (smoking is the major controllable risk factor). There are many so-called putative risk factors where increasing evidence is being gathered as to the exact influence of the factor on the disease. Nutrition and diet is increasingly seen as one modifiable risk factor and patients, spurred on often by less than scientific pronouncements in the popular press, expect us to offer the best advice.
AREDS
The Age Related Eye Disease Study (AREDS) originally set out to look at the influence of factors such as diet and supplementation upon the progression of AMD and cataracts (the latter disease was soon dropped as no evidence was forthcoming of any link). This large multicentre study was the first recognised research programme to establish a significant link between AMD and diet. They reported in the mid-1990s that current AMD patients who had a diet supplemented with vitamins A, C and E along with zinc (and copper to avoid anaemia) were less likely to progress to late-stage AMD in one eye. Macular pigments (lutein and zeaxanthin) were not included in the original supplement as they were not commercially available in such form at the start of the study. AREDS has, however, continued to this day and occasionally produces further papers looking at the role of diet and supplementation on AMD progression.
AREDS report number 22 was published in September's issue of Archives of Ophthalmology and showed the result of supplementation with the same vitamins as before but also with lutein and zeaxanthin. The study reports that the supplementation reduces the risk of AMD progression. More than 4,500 participants were studied, categorised into four AMD severity groups along with a control group in whom less than 15 drusen were found. All were aged between 60 and 80 at enrolment. In commenting on the results, the paper states 'study participants reporting the highest dietary intake of lutein/zeaxanthin were statistically less likely to have advanced AMD (both geographic atrophy and choroidal neovascularisation) or large or extensive intermediate drusen than those reporting lowest dietary intake.' In conclusion, the authors state, 'if these cross-sectional results can be confirmed in prospective samples and experimental studies, lutein and zeaxanthin may be considered as useful agents in food or supplement-based interventions designed to reduce the risk of AMD.'
So, although it would seem that there is a benefit in supplementation for patients already showing AMD in reducing the risk of progression to advanced levels of the disease, the authors are aware that prospective studies are needed before the supplementation is confirmed as preventing the disease altogether.
CERA
And this is what makes the recent paper in the British Medical Journal interesting. A group based at the Centre for Eye Research Australia (CERA) carried out a meta-analysis of nine such prospective studies as well as three randomised controlled studies (involving 149,203 people) to look at the role of dietary antioxidants and supplements in primary prevention of AMD. As such, AREDS, which looked at the influence in established AMD sufferers (and therefore secondary prevention) was not included in the analysis.
They conclude that a range of dietary antioxidants and supplements, including vitamins A, C and E, zinc, lutein and zeaxanthin, a carotene, ß-carotene, ß-cryptoxanthin and lycopene 'have little or no effect' with the exception of vitamin E which showed a 'modest borderline protective association'.
So as practitioners we might conclude that those wishing to avoid AMD later in life should not smoke, but that diet has little direct influence. Once signs of AMD are diagnosed, however, supplementation may reduce the progression of the disease. The CERA authors hypothesise that once early to intermediate AMD has developed, uncontrollable oxidative chain reactions of reactive oxygen species begin and so high antioxidant levels may then be effective in slowing the disease progress. Healthy eyes would not have such a cascade and therefore the influence of antioxidants might be questioned.
The authors highlight that this is an analysis of just nine studies and, as with the AREDS team, it is important for further data to be collated before it can categorically be claimed what the influence of diet is on AMD. Until then, eye care practitioners need to inform patients of the actual state of science at the moment and be wary of some of the more dramatic claims sometimes reported either in the general media or through implication of commercially involved sources.
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