Diabetic retinopathy (DR) is a form of microangiopathy. Reducing oxidative stress in the mitochondria and cell membranes decreases ischemic injury and end-organ damage to the retina. New approaches are needed, which reduce the risk and improve the outcomes of DR while complementing current therapeutic approaches. Homocysteine (Hcy) elevation and oxidative stress are potential therapeutic targets in DR.Common genetic polymorphisms such as those of methylenetetrahydrofolate reductase (MTHFR), increase Hcy and DR risk and severity. Patients with DR have high incidences of deficiencies of crucial vitamins, minerals, and related compounds, which also lead to elevation of Hcy and oxidative stress. Addressing the effects of the MTHFR polymorphism and addressing comorbid deficiencies and insufficiencies reduce the impact and severity of the disease. This approach provides safe and simple strategies that support conventional care and improve outcomes.Suboptimal vitamin co-factor availability also impairs the release of neurotrophic and neuroprotective growth factors. Collectively, this accounts for variability in presentation and response of DR to conventional therapy. Fortunately, there are straightforward recommendations for addressing these issues and supporting traditional treatment plans.We have reviewed the literature for nutritional interventions that support conventional therapies to reduce disease risk and severity. Optimal combinations of vitamins B1, B2, B6, L-methylfolate, methylcobalamin (B12), C, D, natural vitamin E complex, lutein, zeaxanthin, alpha-lipoic acid, and n-acetylcysteine are identified for protecting the retina and choroid. Certain medical foods have been successfully used as therapy for retinopathy. Recommendations based on this review and our clinical experience are developed for clinicians to use to support conventional therapy for DR.DR from both type 1 diabetes mellitus (T1DM) and type 2 diabetes mellitus (T2DM) have similar retinal findings and responses to nutritional therapies.

BackgroundThe aim was to determine retinal nerve fiber layer function and its relations to retinal microvasculature and microcirculation in patients with myopia.MethodPolarization-sensitive optical coherence tomography (PS-OCT) was used to measure phase retardation per unit depth (PR/UD, proportional to the birefringence) of the retinal nerve fiber layer (RNFL). Optical coherence tomography angiography (OCTA) was used to measure macular vessel density analyzed using fractal analysis. In addition, a retinal function imager (RFI) was used to measure macular blood flow velocities in arterioles and venules. Twenty-two patients with moderate myopia (MM, refraction > 3 and < 6 diopters), seventeen patients with high myopia (HM, ≥ 6 D) and 29 healthy control subjects (HC, ≤ 3.00 D) were recruited. One eye of each patient was imaged.ResultsAlthough the average PR/UD of the RNFL in the HM group did not reach a significant level, the birefringence of the inferior quadrant was significantly lower (P < 0.05) in the HM group compared to the HC group. Significant thinning of the average RNFL and focal thinning of RFNL in temporal, superior and inferior quadrants in the HM group were found, compared to the HC group (P < 0.05). There were no significant differences of retinal blood flow velocities in arterioles and venules among groups (P > 0.05). The macular vessel density in both superficial and deep vascular plexuses was significantly lower in the HM group than in the other two groups (P < 0.05) as well as in the MM group than in the HC group (P < 0.05). The average PR/UD and PR/UD in the inferior quadrant were not related to refraction, axial length, blood flow velocities and macular vessel densities (r ranged from − 0.09 to 0.19, P > 0.05).ConclusionsThe impairment of the retinal nerve fiber birefringence in the HM group may be one of the independent features in high myopic eyes, which appeared not to relate to macular microvascular density and blood flow velocity.

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