Diet and Diabetic Retinopathy: Insights From the Diabetes Control and Complications Trial (DCCT)

David K. Cundiff; Claudio R. Nigg, PhD

In This Article

Abstract and Introduction

Objective: We explore the influence of lifestyle on the progression of retinopathy.
Design: Post hoc statistical analysis.
Subjects/Setting: One thousand forty-one patients with type 1 diabetes from 29 specialty clinics.
Intervention: The Diabetes Control and Complications Trial (DCCT) lifestyle data (diet, exercise, and tobacco use) and retinopathy-related risk factors (mean arterial pressure, the low-density lipoprotein/high-density lipoprotein cholesterol ratio [LDL-C/HDL-C], serum triglycerides, glycosolated hemoglobin [HbA1c] levels, body mass index [BMI], and insulin utilization) were related to the rate of progression of retinopathy.
Main Outcome Measures: Correlation between lifestyle data with progression of retinopathy and retinopathy-related risk factors.
Results: The percentage of calories as total fatty acids at baseline and overall positively correlated with prestudy and overall progression of retinopathy (r = .15, P < .0001 and r = .14, P < .0001, respectively). Average overall percentage of calories as dietary fiber inversely correlated with prestudy and overall progression of retinopathy (r = -.07, P = .0102 and r = -.10, P < .0002, respectively). The progression of retinopathy correlated with mean arterial pressure (prestudy r = .09, P = .0004 and overall r = .20, P < .0001), LDL-C/HDL-C (prestudy r = .13, P < .0001 and overall r = .15, P < .0001), serum triglycerides (prestudy r = .18, P < .0001 and overall r = .26, P < .0001), HbA1c (prestudy r = .10, P < .0001 and overall r = .45, P < .0001), BMI (prestudy r = .08, P < .0034 and overall r = .05, P = .08), insulin utilization (prestudy r = .19, P < .0001 and overall r = .14, P < .0001), tobacco use (prestudy r = .08, P < .0231 and overall r = .09, P < .0011), and the intensive vs conventional therapy study group (on-study r = -.27, P < .0001).
Conclusion: Tobacco use and diet, particularly the consumption of fatty acids and dietary fiber, are significantly associated with the rate of progression of diabetic retinopathy and retinopathy-related risk factors.

Previous to 1993, studies had not proven that near-normal glycemia affects the development of retinopathy or other microvascular or macrovascular complications of diabetes.[1,2,3,4,5,6,7,8,9,10] In 1993, the study authors of the Diabetes Control and Complications Trial (DCCT) presented the results and conclusions of their 9-year study, supporting intensive glycemic control to slow the progression of retinopathy, nephropathy, and neuropathy. With a randomized, controlled trial of 1441 patients with type 1 diabetes, an intensive treatment program with close monitoring by the patients and medical personnel was associated with reduced progression of retinopathy (65%), nephropathy (54%), and neuropathy (60%) compared with conventional treatment.[11] The intensive treatment group patients received 3-4 insulin injections per day or a continuous infusion insulin pump, whereas conventionally treated patients had 1 or 2 insulin injections per day. The intensive control group averaged 1.9% lower glycosolated hemoglobin (HbA1c) levels than the conventional treatment group throughout the 6.5-year average follow-up period (HbA1c = 7.2% vs 9.1%, respectively, P < .0001).[11]

These results of the DCCT regarding microvascular complications of patients with type 1 diabetes established the role of near-normal glycemia despite the increased burden on the patient[12] and the additional hypoglycemic risks.[13,14] Since the completion of the DCCT, the risk of hypoglycemia has been significantly reduced with the advent of short-acting insulins.[15]

The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure does not refer to blood pressure control reducing the microvascular complications of diabetes.[16] One observational study found a positive correlation between hypertension and retinopathy.[17] The most recent report of the National Cholesterol Education Program does not mention evidence that lipid-lowering strategies reduce the microvascular complications of diabetes.[18] The American Diabetes Association's (ADA's) "Evidence-Based Nutrition Principles and Recommendations for the Treatment and Prevention of Diabetes and Related Complications" does not specifically address the effects of nutrition on the microvascular complications of diabetes or of nutrition influencing HbA1c. This report observes that low-saturated-fat (ie, < 10% of energy), high-carbohydrate diets increase postprandial levels of plasma glucose but do not state what they do to HbA1c. It reports that high monounsaturated fat diets have not been shown to improve fasting plasma glucose or HbA1c values. It also comments about the strong short-term relationship between total carbohydrate intake and insulin consumption but not the long-term relationship of insulin consumption to any of the macronutrient components.[19]

Among the many complications of overweight and obesity mentioned in the "Surgeon General's call to action to prevent and decrease overweight and obesity," progression of diabetic retinopathy is not mentioned.[20] A position statement by the ADA encourages aerobic exercise in type 1 diabetics but does not reference specific evidence that it slows the progression of diabetic retinopathy.[21] Tobacco has been found to accelerate diabetic retinopathy[17,22,23] and to not be correlated with diabetic microvascular complications.[24] Consequently, the extent of the relationship between diet, exercise, and tobacco use and diabetic retinopathy, either directly or indirectly, via increases in blood pressure, lipids, HbA1c, body mass index (BMI), or insulin utilization has not been determined.

The purpose of this analysis of the DCCT data is to (1) determine the extent to which the intake of macro- and micronutrients of subjects differed by time (ie, baseline vs on-study) and strata (ie, primary prevention and secondary intervention); (2) quantify and compare the influence of retinopathy risk factors (duration of diabetes, blood pressure, serum lipids, HbA1c, treatment group [intensive therapy vs conventional treatment], BMI, insulin utilization, exercise, and tobacco use) on the progression of retinopathy; and (3) calculate the influence of individual dietary variables, exercise, and tobacco use on the progression of retinopathy and on mean arterial pressure, the low-density lipoprotein/high-density lipoprotein cholesterol ratio (LDL-C/HDL-C) ratio, serum triglycerides, HbA1c, BMI, and insulin utilization.


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