An Eye to Health: Diet and Age-Related Macular Degeneration

William C. Ou, BS; Charles C. Wykoff, MD, PhD


June 27, 2017

New Insights Into Dietary Impacts on AMD Development

Two studies published in 2012 reported that a low-GI diet can delay development of retinal lesions that precede AMD in mice.[18,19]

Building on these reports, a 2017 study by Rowan and colleagues[20] explored the ability of a low-GI diet to arrest high-GI diet-induced AMD-like features in mice, seeking to demonstrate a mechanistic link between diet and AMD by examining changes in metabolism and the gut microbiome.

In an effort to model diet-associated effects in mid-to-late adulthood in humans, middle-aged (12 months) mice were fed one of three diets until old age (24 months). The study diets included a low-GI diet (LG), a high-GI diet (HG), or a high-GI diet with a switch to a low-GI diet (HGxoLG) midway through the study.

HG mice developed many age-related features of AMD, including photoreceptor deterioration, retinal pigment epithelium atrophy, and accumulation of basal laminar deposits, whereas such changes appeared to be delayed in LG mice. Most strikingly, retinal damage was arrested or reversed in HGxoLG mice, ultimately making them nearly indistinguishable from LG mice when evaluated histologically. Higher levels of AGEs were found in HG mice than in LG mice, and analysis of plasma and urine metabolic profiles revealed that accumulation of lipids and lipid peroxidation end-products was associated with age-related features of AMD and an HG diet.

Furthermore, the authors demonstrated that the gut microbiome shifts in response to both aging and changes in diet, providing a mechanistic link between diet and metabolite profiles that influence AMD. A number of potential biomarkers for retinal damage were identified, including propionylcarnitine, lysophosphatidylethanolamine, and serotonin, the latter of which appears to be protective.

The authors concluded that changing from an HG to a LG diet, even during maturity, can protect against development of AMD. They also noted that changes in the gut microbiome and metabolome may facilitate these effects.

The strengths of this study include the well-designed experiments and a multifaceted approach to this complex problem. A clear and important limitation of the study, however, is the utilization of a mouse model. Animal models are a crucial part of biomedical research, and mouse models have been particularly instrumental in elucidating risk factors and processes that underlie AMD.[21] Nonetheless, it is an unfortunate reality that findings from animal studies can be difficult to translate into clinical practice, for reasons such as physiologic incompatibility.[22,23] Therefore, while the work of Rowan and colleagues offers much-needed insight into the mechanisms that link diet and AMD, these findings must be studied in humans before they can be used to inform management decisions and patient recommendations.

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