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Diabetic retinopathy is less a disease of the eye and more a disorder of dysregulated angiogenesis. Persistent hyperglycemia reshapes retinal vascular signaling, promoting chronic inflammation, fragile neovascularization, and impaired repair.

Rather than a single pathway going wrong, diabetic retinopathy emerges from a cycle in which damaged blood vessels, stressed retinal cells, and impaired healing reinforce one another over time. Long before vision loss becomes apparent, subtle molecular and structural changes are already reshaping the retinal environment.

A review by Al-Kharashi et al. 2018 highlights the growing global burden of diabetes, reporting that 382 million people were affected worldwide in 2013, with projections estimating this number will reach 592 million by 2035.

One of the earliest and most unifying drivers of diabetic retinal injury is oxidative stress.

Chronically elevated glucose increases the production of reactive oxygen species (ROS), both through direct metabolic pathways and indirectly through the formation of advanced glycation end products (AGEs). When antioxidant defenses are overwhelmed, ROS begin damaging DNA, proteins, lipids, and mitochondria.

Diabetes damages blood vessels everywhere, but retinal vessels are uniquely vulnerable because retinal cells absorb glucose directly and aggressively, experience high metabolic stress, and depend on delicate capillaries that fail quickly under hyperglycemia.

Animal studies consistently show that reducing oxidative stress can preserve retinal structure, normalize inflammatory signaling, and protect capillary cells, highlighting its central role in disease progression.

As capillaries are lost and blood flow becomes irregular, regions of the retina experience chronic hypoxia.

In response, retinal cells attempt to restore oxygen delivery by stimulating new vessel growth, but in diabetes, this repair response is often disordered.

Instead of forming stable, functional vessels, the retina produces fragile, leaky microvessels that worsen edema and tissue injury. Hypoxia, inflammation, and oxidative stress reinforce one another, creating a self-sustaining loop of damage.

While diet cannot treat diabetic retinopathy on its own and blood glucose control remains the first priority, certain foods may help support vascular integrity and balanced angiogenic signaling by improving endothelial function and reducing chronic stress on the microvasculature.

🐟 Omega-3–rich foods → Fatty fish, walnuts, and flaxseed help reduce inflammation and oxidative stress, supporting more stable blood vessel function.

🫐 Polyphenol-rich fruits and vegetables → Berries, leafy greens, onions, and herbs provide antioxidants that modulate inflammatory and angiogenic pathways.

🫜 Nitric oxide–supporting vegetables → Beets, arugula, and spinach support nitric oxide bioavailability, which is essential for healthy blood flow and endothelial health.

🌾 Whole grains and legumes → Oats, barley, lentils, and beans improve glycemic control, helping limit hyperglycemia-driven vascular damage.

Download our Free Guide to learn how to enjoy foods that support angiogenesis.

To learn more, visit our YouTube channel for videos on diabetic retinopathy and weekly new content featuring our mascot, Dr. Angio, who brings complex health and research topics to life.

Best wishes,
- The Angiogenesis Foundation

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