Age-related macular degeneration (AMD) is the leading cause of vision loss in the West, affecting up to 35% of people aged 75 and over. The center of the retina, called the macula, is very rich in photoreceptors, the hyperspecialized cells that capture light and allow us to perceive the details and colors of the world around us.
During macular degeneration, these cells gradually cease to function and there is then a gradual deterioration of vision: difficulty in reading or seeing at a distance, visual distortions (straight lines that become curved), difficulty in distinguishing colors and, ultimately, appearance of a dark spot in the center of vision.
In some cases, AMD is accompanied by vascularization under the retina and these new vessels considerably aggravate the vision problems of those affected. Formed by the process of angiogenesis, these vessels are indeed very fragile and allow blood to filter towards the retina, which can irreversibly damage the photoreceptors and lead to complete blindness.
The retina, a sophisticated and fragile device
What is the signal that causes these new blood vessels to form? Since the photoreceptors located in the macula are very active cells that consume a large amount of oxygen, it can be assumed that the purpose of neovascularization is to supply these cells with the nutrients essential to their functions. AMD would therefore be basically a problem of energy dysregulation at the level of the photoreceptors.
To explore this possibility, a team led by scientists from the University of Montreal and McGill University studied in detail the metabolism of retinal cells and examined its influence on the production of VEGF, a growth factor responsible for the formation of new blood vessels through the process of angiogenesis. They first made the astonishing discovery that the photoreceptors do not only use sugar to meet their energy needs, as previously believed, but also the fats present in the bloodstream. Could an imbalance in the metabolism of these fats explain the increase in vascularization observed in the more severe forms of AMD?
A natural process that turns against us
It seems so. Thanks to a series of experiments, the scientists succeeded in showing that the photoreceptors expressed on their surface a kind of “sensor”, capable of detecting the levels of fat present in the circulation. This mechanism has evolved over the course of evolution to optimize the cell’s energy supply and ensure that good vision can be maintained even in times of starvation (good vision is essential for finding food !).
However, this system does not work well when these levels of fat are high: the sensor believes that there is an overabundance of food and seeks to protect the cell from an excess of energy, for example by preventing it from absorbing sugar. Confronted with this deficiency, the photoreceptor “cries for help” and secretes VEGF to attract new blood vessels to it capable of providing it with the required energy.
In other words, the invasion of the retina by blood vessels is a desperate attempt by the photoreceptors to meet their energy needs in fat and sugar, which unfortunately causes irreversible tissue damage and loss of vision. These observations are very important and could in particular explain why dyslipidemia (too much fat in the blood) is an important risk factor for AMD accompanied by neovascularization.
Prevent AMD through diet
In light of the results of this study, it is certain that the adoption of lifestyle habits that reduce these blood fats can have positive effects on the development of AMD.
An interesting approach is to replace industrial foods (which are often the main source of fat and sugar in our diet) with plants: not only is it better for health in general, but several studies have suggested that compounds Phytochemicals such as carotenoids and polyphenols present in many fruits and vegetables, such as green vegetables or berries, significantly reduce the risk of AMD.
Joyal JS et al. Retinal lipid and glucose metabolism dictates angiogenesis through the lipid sensor Ffar1. Nature Med, 2016; 22: 439-45.