Life Extension is a global authority on nutrition, health and wellness

as well as a provider of scientific information on anti-aging supplements and therapies. We supply only the highest quality nutritional supplements, including minerals, vitamins, herbs and hormones.

HOME

MEMBERSHIP

PRODUCTS

Access your account today: Login Learn about our membership benefits

Life Extension Overstock Sale - Save 60% to 75% - SHOP NOW

Page: 1 | 2 | 3

PDF

Table of Contents

LE Magazine June 2004

Diabetes
Understanding And Preventing The Next Health Care Epidemic
By Lyle MacWilliam, BSc, MSc, FP

The Role of Supplements
Beyond a healthy diet, considerable evidence demonstrates the efficacy of daily nutritional supplementation as a way to prevent and treat diabetes. The following dietary supplements have been found to be particularly beneficial:

Alpha-lipoic acid enhances the breakdown of glucose through intervention at several points along the central metabolic pathway. Supplementation provides a significant boost in glucose disposal and insulin sensitivity.44

Biotin assists in the metabolism of fats, proteins, and carbohydrates, and directly influences blood glucose levels by enhancing glucokinase activity.45 (Glucokinase is an enzyme that controls the first step of glucose oxidation.) Supplementation at high levels significantly improves glucose control and reduces the risk of diabetic neuropathy.46

L-carnitine deficiency is common in diabetics and is associated with cataract formation and cardiomyopathy (weakening of the heart muscle). Supplementation improves insulin sensitivity, in-creases glucose storage, and optimizes carbohydrate metabolism.47 Carnitine also appears to protect against diabetic neuropathy by lowering sorbitol levels in nerve cells.

Carnosine, an amino acid peptide, prevents cross-linking of glucose with proteins (glycation) and arrests the formation of advanced glycation end-products in the cell.48 Glycation accelerates the aging process and is problematic in diabetics. Carnosine also bolsters proteolytic (protein-destroying) pathways to dispose of damaged proteins created through glycation.

Chromium is essential in modulating glucose metabolism and boosting glucose sensitivity.49 It enhances insulin-dependent transport of glucose into the cell, likely by facilitating the binding of insulin to the receptor site. Supplementation at 1000 micrograms per day has been found to markedly reduce insulin resistance.50 As over 90% of adults are deficient in chromium, daily supplementation is warranted.

Coenzyme Q10, an important component of the cell’s central metabolic pathway, enhances cellular energy production and protects cells from damage by free radicals. Japanese researchers cite its ability to boost respiratory chain function in pancreatic beta cells and improve glycemic control.51

Magnesium lowers blood glucose, increases insulin sensitivity, reduces stress response (which promulgates diabetes), and assists in the maintenance of healthy beta cells.52 Low magnesium status is common among type II diabetics53 and is believed to disrupt insulin secretion and the hormone’s capacity to transport glucose. Supplementation has been found to increase the number and sensitivity of cellular insulin receptors50 and to mitigate carbohydrate intolerance.45

N-acetyl-L-cysteine protects pancreatic beta cells from oxidative damage. Free radicals flourish in fatty tissue and when circulating glucose levels are high (two conditions common in insulin resistance syndrome and diabetes). Supple-mentation with N-acetyl-L-cysteine lowers blood sugar levels, protects beta cells from glucose toxicity, and suppresses beta cell death.54

Vitamin C (ascorbic acid) lowers blood glucose, inhibits glycation,55 prevents the accumulation of sorbitol (which causes cataracts), and synergizes and replenishes other antioxidants. By reducing the level of C-reactive protein, ascorbic acid helps quench the inflammatory response in diabetics and lowers cardiovascular risk. Because vitamin C is the principal antagonist for the excessive free-radical activity observed in diabetes, its presence is critical.45 As most diabetics are deficient in this important nutrient, supplementation is essential.

Vitamin E (alpha-tocopherol), a potent lipid-phase antioxidant, quenches lipid peroxidation, increases insulin sensitivity, and enhances glucose transport. High-dose vitamin E supplementation at 1200 milligrams per day has been found to reduce vascular inflammation and lower C-reactive protein levels.56

Vitamin K appears to play an important role in the regulation of blood sugar57 and the reduction of interleukin-6 (IL-6), an inflammatory marker for diabetes; however, people on anticoagulant drugs, such as Coumadin®, should not take vitamin K.

Insulin resistance and diabetes can also be treated successfully with plant-based remedies indigenous to many native cultures. Several herbal remedies are remarkably effective and, unlike drug therapies, have few or no side effects. Hormone therapies, using testosterone and dehydroepiandrosterone (DHEA), show considerable promise.

For a detailed description of these complementary therapies, readers are encouraged to consult the protocols in the Life Extension Foundation’s Disease Prevention and Treatment book,58 as well as Michael Murray’s excellent treatise in his book, Healing Power of Herbs.59

References

1. Diabetes Division, Bureau of Cardio- Respiratory Diseases and Diabetes, Laboratory Centre for Disease Control, Health Protection Branch. Diabetes in Canada: National Statistics and Opportunities for Improved Surveillance, Prevention, and Control. 1999. Health Canada.

2. Diabetes Overview. National Diabetes Information Clearinghouse (NDIC) web- site. November, 2003. Available at: http://diabetes.niddk.nih.gov/dm/pubs/overview/ index.htm. Accessed Jan 31, 2004.

3. Canadian Diabetes Association. About Diabetes: The Prevalence and Costs of Diabetes. Canadian Diabetes Association website. Available at: http://www.diabetes.ca/ Section_About/prevalence.asp. Accessed Jan 31, 2004.

4. McGarry JD. Banting lecture 2001: dysregu- lation of fatty acid metabolism in the etiolo- gy of type 2 diabetes. Diabetes. 2002 Jan;51(1):7-18.

5. Canadian Diabetes Association. Diabetes: impact of disease staggering. Globe and Mail. November 1, 2000: C-1.

6. World Health Organization. Total of People with Diabetes. WHO website. October 31, 2003. Available at: http://www.who.int/ncd/dia/ databases4.htm. Accessed February 2, 2004.

7. Rosenbloom A, Arslanian S, Brink S, et al. Type 2 diabetes in children and adolescents. Diabetes Care. 2000 Mar;23(3):381-9.

8. Rocchini AP. Childhood obesity and a dia- betes epidemic. N Engl J Med. 2002 Mar;346(11):854-5.

9. Widen E, Lehto M, Kanninen T, Walston J, Shuldiner AR, Groop LC. Association of a polymorphism in the beta 3-adrenergic- receptor gene with features of the insulin resistance syndrome in Finns. N Engl J Med. 1995 Aug;333(6):348-51.

10. Grundy SM, Howard B, Smith S Jr, Eckel R, Redberg R, Bonow RO. Prevention Conference VI: Diabetes and Cardiovascular Disease: executive summary: conference proceeding for healthcare pro- fessionals from a special writing group of the American Heart Association. Circulation. 2002 May;105(18):2231-9.

11. Stagnitti MN. Statistical Brief #34: The Prevalence of Obesity and Other Chronic Health Conditions among Diabetic Adults in the U.S. Community Population, 2001. Medical Expenditure Panel Survey. Agency for Healthcare Research and Quality, Department of Health and Human Services webpage. Available at: http://www.meps.ahrq.gov/PrintProducts/ PrintProd_Detail.asp. Accessed Jan 30, 2004.

12. Neel JV. Diabetes mellitus: a “thrifty” genotype rendered detrimental by “progress”? Am J Hum Genet. 1962 Dec;14:353-62.

13. Minokoshi Y, Kim YB, Peroni OD, et al. Leptin stimulates fatty-acid oxidation by activating AMP-activated protein kinase. Nature. 2002 Jan;415(6869):339-43.

14. Deus P. Leptin: The next big thing. Mind and Muscle Magazine [serial online]. Oct 26, 2001; Issue 3. Available at: http://mindand muscle.net/magazine/i3leptin.html. Accessed February 12, 2004.

15. Sinha MK, Caro JF. Clinical aspects of lep- tin. Vitam Horm. 1998;54:1-30.

16. Eiden S, Daniel C, Steinbrueck A, Schmidt I, Simon E. Salmon calcitonin—a potent inhibitor of food intake in states of impaired leptin signalling in laboratory rodents. J Physiol. 2002 Jun;541(Pt 3):1041-8.

17. Astrup A, Buemann B, Christensen NJ, Toubro S. Failure to increase lipid oxidation in response to increasing dietary fat content in formerly obese women. Am J Physiol. 1994 Apr;266(4 Pt 1):E592-E599.

18. Froidevaux F, Schutz Y, Christin L, Jequier E. Energy expenditure in obese women before and during weight loss, after refeed- ing, and in the weight-relapse period. Am J Clin Nutr. 1993 Jan;57(1):35-42.

19. Ravussin E, Lillioja S, Knowler WC, et al. Reduced rate of energy expenditure as a risk factor for body-weight gain. N Engl J Med. 1988 Feb;318(8):467-72.

20. Man ZW, Hirashima T, Mori S, Kawano K. Decrease in triglyceride accumulation in tis- sues by restricted diet and improvement of diabetes in Otsuka Long-Evans Tokushima fatty rats, a non-insulin-dependent diabetes model. Metabolism. 2000 Jan;49(1):108-14.

21. Ohneda M, Inman LR, Unger RH. Caloric restriction in obese pre-diabetic rats prevents beta-cell depletion, loss of beta-cell GLUT 2 and glucose incompetence. Diabetologia. 1995 Feb;38(2):173-9.

22. Sattar N, Gaw A, Scherbakova O, et al. Metabolic syndrome with and without C- reactive protein as a predictor of coronary heart disease and diabetes in the West of Scotland Coronary Prevention Study. Circulation. 2003 Jul;108(4):414-9.

23. Faloon W. What you don’t know about blood sugar. Life Extension Magazine. January 2004:11-20.

24. Bjornholt JV, Erikssen G, Aaser E, et al. Fasting blood glucose: an underestimated risk factor for cardiovascular death. Results from a 22-year follow-up of healthy nondia- betic men. Diabetes Care. 1999 Jan;22(1):45-49.

25. Harris MI, Hadden WC, Knowler WC, Bennett PH. Prevalence of diabetes and impaired glucose tolerance and plasma glu- cose levels in US population aged 20-74 yr. Diabetes. 1987 Apr;36(4):523-34.

26. Mayfield J. Diagnosis and classification of diabetes mellitus: new criteria. Am Fam Physician. 1998 Oct;58(6):1355-70.

27. Allison DB, Fontaine KR, Manson JE, Stevens J, VanItallie TB. Annual deaths attributable to obesity in the United States. JAMA. 1999 Oct;282(16):1530-8.

28. Mokdad AH, Ford ES, Bowman BA, et al. Prevalence of obesity, diabetes, and obesity- related health risk factors, 2001. JAMA. 2003 Jan;289(1):76-9.

29. Hu FB, Manson JE, Stampfer MJ, et al. Diet, lifestyle, and the risk of type 2 diabetes mel- litus in women. N Engl J Med. 2001 Sep;345(11):790-7.

30. Knowler WC, Barrett-Connor E, Fowler SE, et al. Reduction in the incidence of type 2 diabetes with lifestyle intervention or met- formin. N Engl J Med. 2002 Feb;346(6):393-403.

31. Lemieux I, Pascot A, Prud’homme D, et al. Elevated C-reactive protein: another compo- nent of the atherothrombotic profile of abdominal obesity. Arterioscler Thromb Vasc Biol. 2001 Jun;21(6):961-7.

32. Heilbronn LK, Noakes M, Clifton PM. Energy restriction and weight loss on very- low-fat diets reduce C-reactive protein con- centrations in obese, healthy women. Arterioscler Thromb Vasc Biol. 2001 Jun;21(6):968-70.

33. Challem J, Berkson B, Smith M. Syndrome X. New York: John Wiley & Sons; 2000.

34. Reaven GM. Syndrome X. New York: Simon and Schuster; 2000.

35. Salmeron J, Hu FB, Manson JE, et al. Dietary fat intake and risk of type 2 diabetes in women. Am J Clin Nutr. 2001 Jun;73(6):1019-26.

36. Chandalia M, Garg A, Lutjohann D, von Bergmann K, Grundy SM, Brinkley LJ. Beneficial effects of high dietary fiber intake in patients with type 2 diabetes mellitus. N Engl J Med. 2000 May;342(19):1392-8.

37. Greiger L. Syndrome X. Heart Information Network webpage. Available at: http://www.heartinfo.com/nutrition/ syndx072999.htm. Accessed Nov 15, 2000.

38. Helmrich SP, Ragland DR, Leung RW, Paffenbarger RS, Jr. Physical activity and reduced occurrence of non-insulin-depen- dent diabetes mellitus. N Engl J Med. 1991 Jul;325(3):147-52.

39. Manson JE, Rimm EB, Stampfer MJ, et al. Physical activity and incidence of non- insulin-dependent diabetes mellitus in women. Lancet. 1991 Sep;338(8770):774-778.

40. Manson JE, Nathan DM, Krolewski AS, Stampfer MJ, Willett WC, Hennekens CH. A prospective study of exercise and inci- dence of diabetes among US male physi- cians. JAMA. 1992 Jul;268(1):63-7.

41. Uusitupa M, Louheranta A, Lindstrom J, et al. The Finnish Diabetes Prevention Study. Br J Nutr. 2000 Mar;83(Suppl 1):S137-42.

42. Nieman DC. Fitness and Sports Medicine. 3rd ed. Palo Alto, CA: Bull Publishing; 1995.

43. Diabetes Type II and the Syndrome X Connection. Life Extension Foundation website. Available at: http://www.lef.org/protocols/prtcls-text/t-prctl-042.html. Accessed Jan 27, 2004.

44. Jacob S, Streeper RS, Fogt DL, et al. The antioxidant alpha-lipoic acid enhances insulin-stimulated glucose metabolism in insulin-resistant rat skeletal muscle. Diabetes. 1996 Aug;45(8):1024-9.

45. Murray MT. Encyclopedia of Nutritional Supplements. Rocklin, CA: Prima Publishing; 1996.

46. Koutsikos D, Agroyannis B, Tzanatos- Exarchou H. Biotin for diabetic peripheral neuropathy. Biomed Pharmacother. 1990;44(10):511-4.

47. Crayhon R. The Carnitine Miracle. New York: M. Evans; 1999.

48. Hipkiss AR, Brownson C. A possible new role for the anti-ageing peptide carnosine. Cell Mol Life Sci. 2000 May;57(5):747-53.

49. McCarty MF. Toward a wholly nutritional therapy for type 2 diabetes. Med Hypotheses. 2000 Mar;54(3):483-7.

50. Diabetes Type II and the Syndrome X Connection. Life Extension Foundation website. Available at: http://www.lef.org/ protocols/prtcls-text/t-prctl-042.html. Accessed Jan 27, 2004.

51. McCarty MF. Can correction of sub-optimal coenzyme Q status improve beta-cell func- tion in type II diabetics? Med Hypotheses. 1999 May;52(5):397-400.

52. Kowluru A, Chen HQ, Modrick LM, Stefanelli C. Activation of acetyl-CoA car- boxylase by a glutamate-and magnesium- sensitive protein phosphatase in the islet beta-cell. Diabetes. 2001 Jul;50(7):1580-7.

53. Paolisso G, Passariello N, Pizza G, et al. Dietary magnesium supplements improve B- cell response to glucose and arginine in elderly non-insulin dependent diabetic sub- jects. Acta Endocrinol (Copenh). 1989 Jul;121(1):16-20.

54. Kaneto H, Kajimoto Y, Miyagawa J, et al. Beneficial effects of antioxidants in diabetes: possible protection of pancreatic beta-cells against glucose toxicity. Diabetes. 1999 Dec;48(12):2398-2406.

55. Emekli N. Nonenzymatic glycosylation of tis- sue and blood proteins. J Marmara Univ Dent Fac. 1996 Sep;2(2-3):530-534.

56. Devaraj S. Vitamin E shows promise in treating diabetes. Washington, DC: Hearst Newspapers. June 5, 2001. Available at: http://www.ithyroid.com/diabetes.htm. Accessed January 27, 2004.

57. Sakamoto N, Nishiike T, Iguchi H, Sakamoto K. Relationship between acute insulin response and vitamin K intake in healthy young male volunteers. Diabetes Nutr Metab. 1999 Feb;12(1):37-41.

58. Segala M, ed. Disease Prevention and Treatment. 4th ed. Hollywood, FL: Life Extension Media; 2003.

59. Murray MT. Healing Power of Herbs. 2nd ed. Rocklin, CA: Prima Publishing; 1995.

Better Business Bureau Accredited Business

Life Extension Royal Treatment Customer Service

*These statements have not been evaluated by the FDA. These products are not intended to diagnose, treat, cure, or prevent any disease.

The information provided on this site is for informational purposes only and is not intended as a substitute for advice from your physician or other health care professional or any information contained on or in any product label or packaging. You should not use the information on this site for diagnosis or treatment of any health problem or for prescription of any medication or other treatment. You should consult with a healthcare professional before starting any diet, exercise or supplementation program, before taking any medication, or if you have or suspect you might have a health problem. You should not stop taking any medication without first consulting your physician.