The problem with diabetes is that we desperately need to avoid or reduce the complications but know as well that there is a disconnect between blood sugar control and the development of the complications (1). We also know that there is evidence that the complications may be caused, at least in part, by the continuing autoimmune processes which caused the initial beta cell destruction in type 1 diabetes turning their attack on other parts of the body (2), as well as by genetic influences inherited along with the genes which predispose the patient to developing diabetes (3). So if even strict blood sugar control may not protect us from complications, what are we to do?
Well, there are numerous studies indicating that some supplements may prevent or slow the development of complications. Some of these studies are experimental (i.e., conducted in animals), while others are tentative in their conclusions, but some are more affirmative in their assertion of the benefit of supplements in keeping diabetic complications at bay (4). What should we sensibly do, when faced with the demonstrated inadequacy of strict blood sugar control to prevent the development of complications on the one hand, and the possibility of supplements helping in this struggle? I think it is rational to try supplementation when faced with the fact that we have diabetes now and can’t wait another 20 or 30 years for the research indicating the benefit of supplements to be finalized, in the plodding, hesitant, ultra-conservative style of medical inference. The logical mechanism behind much of the protective effect of supplements on diabetic complications relates to the action of hyperglycemia in promoting inflammation to produce complications, since many of the interventions recommended suppress inflammation (5).
(1) J. Chan, et al., “Diabetic Nephropathy and Proliferative Retionpathy with Normal Glucose Tolerance,” Diabetes Care, 8 (4) 385-390 (1985); J. Estenes, “Absence of Diabetic Retinopathy in a Patient Who Has Had Diabetes Mellitus for 69 Years and Inadequate Glycemic Control,” Diabetology and Metabolic Syndrome, 1 (13), October 5, 2009; C. Huang, “RCa3.1: A New Player in Progressive Kidney Disease,” Current Opinion in Nephrology and Hypotension, 24 (1) 61-66 (2015); R. Mactier, et al., “Diabetic Glomerulosclerosis Without Concurrent Diabetes Mellitus,” Southern Medical Journal, 81 (12) 1573-1577 (1988); S, Rich, “Genetics of Diabetes and Its Complications,” Journal of the American Society of Nephrology, 17, 353 (2006); R. Semba, et al., “The Role of GbcNAc Signaling in the Pathogenesis of Diabetic Retinopathy,” Proteomics Clinical Applications, 8 (3-4) 218-221 (2014); A. Sima, “Pathological Mechanism Involved in Diabetic Nephropathy: Can We Slow the Process?” Current Opinion in Investigational Drugs, 7 (4) 334-337 (2006).
(2) D. Adams, “Autoimmune Destruction of Pericytes as the Cause of Diabetic Retinopathy,” Clinical Ophthalmology, 2 (2) 295 (2008); C. De Souza, et al., “Consumption of a Fat-Rich Diet Activates a Proinflammatory Response and Induces Insulin Resistance,” Endocrinology, 146 (10) 4192; V. Granberg, et al., “Autoantibodies to Autonomic Nerves Associated with Cardiac and Peripheral Autonomic Neuropathy,” Diabetes Care, 28 (8) 1959 (2005); A. Vinik, et al., “Antibodies to Neuronal Structures,” Diabetes Care, 26 (8) 2067 (2005).
S. Abharu, et al., “A Systematic Meta-Analysis of Genetic Association Studies fir Diabetic Retinopathy,” Diabetes, 58 (9) 2137 (2009); K. Hietala, et al., “Heritability of Proliferative Diabetic Retinopathy,” Diabetes , 57 (8) 2176 (2008); R. Leslie, et al., “Level of Advanced Glycated End Product is Genetically Determined,” Diabetes, 52 (9) 2441 (2003); A. Mollstein, et al., “The Endothelial Nitric Oxide Synthase Gene and Risk of Diabetic Nephropathy,” Molecular Genetics and Metabolism, 97 (1) 80 (2009); R. Mueller, et al., “Genetics of Kidneys in Diabetes,” Journal of the American Society of Nephrology, 17 (7) 1783 (2006); M. Monti, et al., “Familial Risk Factors for Microvascular Complications,” Journal of Clinical Endocrinology and Metabolism, 92 (112), 4650 (2007); C. Thorn, et al., “Clustering of Risk Factors in Parents of Patients with Type 1 Diabetes and Nephropathy,” Diabetes Care, 30 (5) 1162 (2007).
Di Leo, et al., “Potential Therapeutic Effect of Antioxidants in Experimental Diabetic Retina: A Comparison between Chronic Taurine and Vitamin E Plus Selenium Supplementation,” Free Radical Research, 37 (3) 323 (2003); R. Fardoun, “The Use of Vitamin E in Type 2 Diabetes Mellitus,” Clinical and Experimental Hypertension, 29 (3) 135 (2007); T. Osawa and Y. Kato, “The Protective Role of Antioxidative Food Factors in Oxidative Stress Caused by Hyperglycemia,” Annals of the New York Academy of Science, 1043, 440 (2005); R. Pazdro and J. Burgess, “The Role of Vitamin E and Oxidative Stress in Diabetic Complications,” Mechanisms of Ageing and Development, 131 (4) 276 (2010); T. Perapatidit, et al., “Plasma Lipid Peroxidation and Antioxidant Nutrients in Type 2 Diabetes Patients,” Journal of the Medical Association of Thailand, 89, Supplement 5, S147-S155 (2006); F. Yulok, et al., “Effects of Stobadine and Vitamin E in Diabetes Induced Retinal Abnormalities,” Archives of Medical Research, 38 (5) 509.
E. g., M. Haidara, et al., 'The Role of Oxidative Stress in Development of Cardiovascular Complications in Diabetes Mellitus," Current Vascular Pharmacology, 4 (3) 215-227 (2006).