Nutrition for diabetic retinopathy: plummeting the inevitable threat of diabetic vision loss.

Diabetic retinopathy (DR) is among the leading causes of preventable blindness. Hyperglycemia, hypertension, hyperlipidemia and anemia majorly predispose its pathogenesis. The current treatment modalities of DR include laser photocoagulation therapy, intravitreal corticosteroids, intravitreal anti-vascular endothelial growth factor (VEGF) agents and vitreo-retinal surgery which are costly, highly invasive, unproven for prolonged use and opted in advanced stages of DR. By then retina already encounters a vast damage. Nutrients by their natural physiological, biochemical and molecular action can preserve retinal structure and functions by interfering with the various pathological steps prompting DR incidence, thereby altering the risk of developing this ocular morbidity. Nutrients can also play a central role in DR patients resistant towards the conventional medical treatments. However due to the byzantine interplay existing between nutrients and DR, the worth of nutrition in curbing this vision-threatening ocular morbidity remains silent. This review highlights how nutrients can halt DR development. A nutritional therapy, if adopted in the initial stages, can provide superior-efficacy over the current treatment modalities and can be a complementary, inexpensive, readily available, anodyne option to the clinically unmet requirement for preventing DR. Assessment of nutritional status is presently considered relevant in various clinical conditions except DR. Body Mass Index (BMI) conferred inconclusive results in DR subjects. Subjective Global Assessment (SGA) of nutritional status has recently furnished relevant association with DR status. By integrating nutritional strategies, the risk of developing DR can be reduced substantially. This review summarizes the subsisting knowledge on nutrition, potentially beneficial for preventing DR and sustaining good vision among diabetic subjects.

Apolipoprotein A-I and B and Subjective Global Assessment relationship can reflect lipid defects in diabetic retinopathy.

OBJECTIVE: Elevated lipid levels increase complications of diabetic retinopathy (DR). Uncontrolled diabetes increases these complications and causes unintentional weight loss, indicating an apparently normal body mass index (BMI). Thus, it is easy to assume that patients with DR and a normal BMI have optimal lipid status. Apolipoprotein (Apo) A-I and Apo B levels differentially indicate serum lipid status in DR. Subjective Global Assessment (SGA) scores are associated with DR status. If SGA scores and serum Apo A-I and B levels are found to be interrelated, their relationship can reflect lipid defects in patients with DR despite apparently normal BMI. The aim of the present study was to investigate the possible relationship between serum Apo A-I and B levels and SGA scores of patients with DR. METHOD: This was a case-control study conducted from November 2011 to April 2014. Serum Apo A-I and B levels and SGA scores were calculated for 40 healthy controls, 48 individuals without DR, 49 nonproliferative DR cases, and 48 proliferative DR cases. Pearson's correlation analysis was applied between Apo A-I, Apo B, Apo B/Apo A-I ratio, and SGA scores. RESULTS: Negative correlation was observed between serum Apo A-I level (r = -0.567, P < 0.001) and positive correlation between serum Apo B level (r = 0.451, P < 0.001) and Apo B/Apo A-I ratio (r = 0.597, P < 0.001) with escalating SGA scores. CONCLUSION: To our knowledge, this is the first study to report a novel correlation between serum Apo A-I, Apo B and Apo B/Apo A-I ratio and SGA scores. SGA scores can help predict lipid abnormalities in patients with DR even when they have an apparently normal BMI.

Interrelationship of elevated serum Advanced Glycation End-product levels and malnutrition (Subjective Global Assessment) scores with the severity of retinopathy in type II diabetes.

BACKGROUND AND AIMS: Hyperglycemia in diabetes causes endogenous formation of Advanced Glycation End-products (AGEs) which accumulate in various body parts including retina causing diabetic retinopathy. AGEs also originate from exogenous dietary sources contributing to the body's AGE pool. Currently, curing of diabetic retinopathy is mainly focused on medication, surgical or laser interventions and not much emphasis is given on preventing or halting its occurrence or advancement to more severe stages, nutritionally. Planning a 'low glycemic index-low AGE' diet therapy for diabetic subjects can reduce endogenous and exogenous origin AGEs in the body and help in controlling retinopathy. Sound and accurate assessment of nutritional status is a crucial step for planning a therapeutic diet for this condition. As this aspect has not gained sufficient attention till now we are assessing the association of serum Advanced Glycation End-product (AGE) levels with the severity of diabetic retinopathy and for the first time estimating the nutritional status of subjects with this eye disorder for long term patient care. METHODS: This was a tertiary care centre-based, case-control study involving sixty three consecutive cases with diabetes divided as 21 cases with diabetes but no retinopathy, 21 cases with non proliferative diabetic retinopathy (NPDR), 21 cases with proliferative diabetic retinopathy (PDR) along with 21 healthy controls. Serum AGE levels of all the cases and controls were evaluated by Enzyme Linked Immuno Sorbent Assay (ELISA) and nutritional status was assessed by anthropometric measurements and SGA scores. RESULTS: Serum AGE levels were found significantly elevated in PDR group when compared with no retinopathy (p < 0.05) and control (p < 0.001) group. Control group was also significantly different from (p < 0.05) from NPDR group. Increase in SGA scores was statistically significant amongst the four study groups though other indices of nutritional status showed no definite trend with the increasing severity of retinopathy. CONCLUSION: Our study shows that serum AGE levels are potential risk markers of diabetic retinopathy and SGA can be used as a regular tool for the assessment of nutritional status of diabetic retinopathy subjects which will help planning a 'low glycemic index-low AGE' therapeutic diet for halting this morbidity.

Advanced glycation end products and diabetic retinopathy.

Studies have established hyperglycemia as the most important factor in the progress of vascular complications. Formation of advanced glycation end products (AGEs) correlates with glycemic control. The AGE hypothesis proposes that hyperglycemia contributes to the pathogenesis of diabetic complications including retinopathy. However, their role in diabetic retinopathy remains largely unknown. This review discusses the chemistry of AGEs formation and their patho-biochemistry particularly in relation to diabetic retinopathy. AGEs exert deleterious effects by acting directly to induce cross-linking of long-lived proteins to promote vascular stiffness, altering vascular structure and function and interacting with receptor for AGE, to induce intracellular signaling leading to enhanced oxidative stress and elaboration of key proinflammatory and prosclerotic cytokines. Novel anti-AGE strategies are being developed hoping that in next few years, some of these promising therapies will be successfully evaluated in clinical context aiming to reduce the major economical and medical burden caused by diabetic retinopathy.