Diabetes Mellitus: Present and Future Preventive Strategies—Part I This is the first in a continuing series of articles
- Thu, 1/17/08 - 4:16am
- 0 Comments
- 2226 reads
Pages 30 - 37
Diabetes mellitus is a growing concern for the older person. All too often undiagnosed and inappropriately treated, diabetes affects approximately 8% of persons over the age of 65 years and more than 20% of those over age 80. We have come a long way in our understanding of the pathogenesis of this life-threatening and potentially debilitating illness, and new methods of treatment continually become available. Preventing complications of diabetes depends largely on controlling the level of blood sugar, although even with good control certain end-organ effects may be inevitable. Clearly, the best way to impact on this problem is to prevent its development in the first place. This article reviews ways in which diabetes mellitus may be prevented, both in terms of reducing its impact on one’s health, as well as methods that might prevent the development of this disease entirely.
HISTORICAL BACKGROUND
Diabetes mellitus was first described in ancient Egypt. Aretaeus named it in the 1st century ad. Galenus spoke of diabetes in the 2nd century and blamed it on “kidney weakness.” Over the next few centuries, numerous theories attempted to explain its origin and sequellae. Paracelsus in the 16th century noted the presence of a “salt” in the evaporated urine of persons with diabetes, and Thomas Willis advocated tasting urine as part of an examination, claiming that the urine of persons with diabetes tasted “wonderfully sweet, as if imbued with honey or sugar.” In 1775, Mathew Dobson identified the “salt-like” material in diabetic urine as sugar, and in 1815 this was further identified as glucose. Over the years, a variety of treatments for persons with diabetes were used, including starvation. Alkalis were added to the treatment regimen and soon antimony, cathartics, and even opium were tried. In 1848, Claude Bernard found sugar in the hepatic veins of dogs who were fed either sugar or protein. After finding glycogen in the liver, he reported that the body could synthesize its own chemicals, and postulated that diabetes resulted from an overproduction of sugar by the liver. He also reported a renal threshold for glucose above which glycosuria resulted. In the latter part of the 19th century, Bouchardat introduced exercise as an adjunct to carbohydrate restriction.
Dr. Frederick Allen advocated the use of “undernutrition” and demonstrated that weight loss due to “caloric restriction and without glycosuria” was beneficial to the adult person with diabetes who is overweight; he claimed that those who complied with his treatment strategy would have longer lives. Patients who lost a similar amount of weight but who still had glycosuria, however, reportedly did worse and continued to have progressive systemic changes.
In 1893, the French histologist Gustave Languesse suggested that the pancreatic islets of Langerhans had an endocrine function. Oscar Minkowski noted that animals that had their pancreas removed became diabetic. In the summer of 1921, Frederick Banting and Charles Best discovered insulin. On January 11, 1922, Leonard Thompson, a 14-year-old boy with diabetes, received the first extract of insulin, opening a new era for treatment. In 1936, H. C. Hagedorn discovered that when protamine was added to the insulin mixture, there was a dramatic increase in the duration of action to about 24 hours, prolonged even further to 36 hours when zinc was added.
Diabetes soon became a model of study for those interested in the field of aging. It was noted that persons with diabetes had more atherosclerosis, claudication, thickening of their basement membranes, renal changes, and neuropathies; these same findings were also noted to occur at higher rates in older individuals. It was theorized that persons with diabetes exhibited an acceleration of the aging process, something that would affect everyone eventually.
REFERENCES 1. Flegal KM, Carroll MD, Ogden CL, Johnson CL. Prevalence and trends in obesity among U.S. adults, 1999-2000. JAMA 2002;288:1723-1727. 2. Mokdad AH, Ford ES, Bowman BA, et al. Diabetes trends in the U.S.: 1990-1998. Diabetes Care 2000;23:1278-1283. 3. Franz MJ, Bantle JP, Beebe CA, et al. American Diabetes Association. Evidence-based nutrition principles and recommendations for the treatment and prevention of diabetes and related complications. Diabetes Care 2003;26(suppl 1):S51-S61. 4. Williamson DF, Thompson TJ, Thun M, et al. Intentional weight loss and mortality among overweight individuals with diabetes. Diabetes Care 2000;23:1499-1504. 5. Muscelli E, Mingrone G, Camastra S, et al. Differential effect of weight loss on insulin resistance in surgically treated obese patients. Am J Med 2005;118:51-57. 6. Allen FM, Stillman E, Fitz R. Exercise (monograph 11). New York: Rockefeller Institute of Medical Research,1919;486-499.7. Frisch RE, Wyshak G, Albright TE, et al. Lower prevalence of diabetes in female former college athletes compared with nonathletes. Diabetes 1986;35:1101-1105. 8. Tsuneki H, Ishizuka M, Terasawa M, et al. Effect of green tea on blood glucose levels and serum proteomic patterns in diabetic (db/db) mice and on glucose metabolism in healthy humans. BMC Pharmacol 2004;4(1):18. 9. Evans JL, Goldfine ID. Alpha-lipoic acid: A multifunctional antioxidant that improves insulin sensitivity in patients with type 2 diabetes. Diabetes Technol Ther 2000;2(3):401-413. 10. Jacob S, Henriksen EJ, Tritschler HJ, et al. Improvement of insulin-stimulated glucose-disposal in type 2 diabetes after repeated parenteral administration of thioctic acid. Exp Clin Endocrinol Diabetes 1996;104(3):284-288. 11. Ziegler D, Hanefeld M, Ruhnau KJ, et al. Treatment of symptomatic diabetic peripheral neuropathy with the anti-oxidant alpha-lipoic acid. A 3-week multicentre randomized controlled trial (ALADIN Study). Diabetologia 1995;38(12):1425-1433. 12. Jones CL, Gonzalez V. Pyridoxine deficiency: A new factor in diabetic neuropathy. J Am Podiatry Assoc 1978;68(9):646-653. 13. Koutsikos D, Agroyannis B, Tzanatos-Exarchou H. Biotin for diabetic peripheral neuropathy. Biomed Pharmacother 1990; 44(10):511-514. 14. Devamanoharan PS, Henein M, Morris S, et al. Prevention of selenite cataract by vitamin C. Exp Eye Res 1991;52(5):563-568. 15. Anderson R, Cheng N, Bryden N, et al. Beneficial effect of chromium for people with type II diabetes. Diabetes 1996;45 (suppl 2):124A. 16. Hambidge KM. Chromium nutrition in man. Am J Clin Nutr 1974;27(5):505-514. 17. Norbiato G, Bevilacqua M, Meroni R, et al. Effects of potassium supplementation on insulin binding and insulin action in human obesity: Protein-modified fast and refeeding. Eur J Clin Invest 1984;14(6):414-419. 18. Davey Smith G, Bracha Y, Svendsen KH, et al. Incidence of type 2 diabetes in the randomized Multiple Risk Factor Intervention Trial. Ann Intern Med 2005;142:313-322. 19. Ivorra MD, Paya M, Villar A. A review of natural products and plants as potential antidiabetic drugs. J Ethnopharmacol 1989;27(3):243-275. 20. Murray MT. Are botanical medicines useful in diabetes? The American Journal of Natural Medicine 1994;1(3):5-7. 21. Sotaniemi EA, Haapakoski E, Rautio A. Ginseng therapy in non-insulin-dependent diabetic patients. Diabetes Care 1995; 18(10):1373-1375.







