What is Type II Diabetes Mellitus?

By: Joseph Pizzorno, ND, Chairman, Scientific Advisory Board
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Type II Diabetes Mellitus

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What is Type II Diabetes Mellitus? 

Type II diabetes mellitus (T2D) is a disease characterized by the progressive worsening of glycemic control, which often starts with mild elevations in blood glucose levels after eating, and, over time, leads to an increase in fasting plasma glucose. Cardiovascular disease is the main cause of morbidity and mortality among diabetic patients, but other complications include nephropathy, neuropathy, and retinopathy, as many types of tissues are damaged by hyperglycemia and the resultant oxidative damage.

It is well established that hyperglycemia is the result of two major defects: a loss of hepatic and peripheral insulin sensitivity, and defective pancreatic ß-cell function. As ß-cell function declines, insulin production is not sufficient to keep up with rising blood glucose levels, and hyperglycemia occurs even when fasting.

Hepatic insulin resistance is marked by an inappropriately high rate of hepatic glucose production, despite elevated insulin concentrations. The inability of endogenous insulin to increase plasma glucose uptake by peripheral tissues indicates peripheral insulin resistance. It is estimated that by the time of diagnosis with T2D, ß-cell function may already be reduced by 50%, marked by an earlier phase of gradual decline and decompensation preceding overt diabetes. This is followed by a phase of rapid acceleration of impaired insulin secretion and ß-cell apoptosis, perhaps due to glucose and lipotoxicity.1 (See Figure 1)

figure 01

How Common Is It? 

The NHANES 1999-2004 found that 7.8% of the total US adult population had diabetes mellitus, and approximately 90-95% of those individuals have been estimated to have T2D.2 In 2005–2006 this estimate had reached 12.9% among people aged >20 years, of which ~40% was undiagnosed.3 The total health care costs attributed to diabetes and related complications reached $174 billion (USD) for the year 2007.4

What may be just as alarming is the increasing prevalence of prediabetes, which is an intermediate stage between normal glucose levels and T2D, defined as either an elevated fasting blood glucose or impaired glucose tolerance that falls short of the criteria for diabetes. The NHANES 2005–2006 found that in people aged > or =20 years, the crude prevalence of impaired fasting glucose was 25.7% and of impaired glucose tolerance was 13.8%, with almost 30% having either. Thus, over 40% of individuals had diabetes or prediabetes.

Why Does It Occur? 

Although there are genetic components to T2D, it is largely thought to occur as a result of poor food choices and physical inactivity. Obesity has been well established as a risk factor for T2D, with both body bass index (BMI) and waist circumference positively associated with the incidence of T2D, with a risk increase of 1.6 to 2.66 fold.5 Given the importance of central adiposity to insulin resistance, it is no surprise that the waist-to-height ratio may also be the best discriminator of cardiovascular disease.6

A diet that is high in refined carbohydrates, with low intakes of fruits, vegetables, legumes, whole grain, and fibre is the pattern associated with the greatest risk.7,8,9 Consistent with this pattern is a diet low in antioxidants that is calorie-rich and nutrient-poor, with a high glycemic index. Although a number of genes have been identified that increase the risk of T2D, the importance of lifestyle is clearly shown by the example of the Pima Indians. This population has the highest rate known rate of T2D, with a strong genetic component. However, Pima Indians living in Mexico have a prevalence of T2D of 6.9%, less than one-fifth of that in the US Pima Indians (38%), due to differences in lifestyle.10

How is it Diagnosed and Monitored? 

The diagnosis of T2D can be made in one of three ways – a fasting plasma glucose =126mg/dL, symptoms of hyperglycemia with a random glucose =200mg/dL, or a 2-hour plasma glucose =200mg/dL during an oral glucose tolerance test (See Table 1).

figure 02

Although fasting glucose alone is often used as a screen for diabetes, it is thought to miss approximately 30% of cases.11 It is an insensitive screen because it does not reflect the earlier rises in postprandial glycemia associated with poor glucose tolerance. Only after the ß-cell function has declined enough for an elevated fasting glucose will these patients be detected, after the disease has progressed. Additionally, patients with both impaired fasting glucose and impaired glucose tolerance develop diabetes twice as often as those with only one of these abnormalities, emphasizing the importance of these tests for prognosis.

Monitoring of T2D patients is primarily done in two ways, by measurement of glycosylated hemoglobin (HbA1c), and by self-monitoring of blood glucose (SMBG). The HbA1c gives an estimate of the average value for blood glucose over the last several months, and is often used to measure the effectiveness of therapy. Very recently, an International Expert Committee has also recommended the use of HbA1c for the diagnosis of diabetes, with a level > or = to 6.5% to be used as the cut-off for diabetes. However, an HbA1c does not give good data for the daily fluctuation of blood sugar – it misses the sharp rises and drops in blood sugar associated with meals that more close monitoring measures.12

What has emerged is the importance of SMBG for better metabolic control in diabetic patients. Additionally, newer technologies have also created the ability to monitor glucose continually, known as continuous glucose monitoring (CGM). It has been shown to have the following benefits compared to SMBG:

  • The ability to detect postprandial glucose excursions;
  • Detection of nocturnal hypoglycemia or hyperglycemia not previously detected by SMBG, even in patients whose HbA1c values suggest reasonably good control. (See Figure 2)13;
  • Allows for patients to have better metabolic control, because the data generated by CGM show the effect of meal choices, missed medication, and the effect of lifestyle on glucose control.

Complications 

Because patients with diabetes are at high risk for a number of other complications, regular evaluation of kidney function, cardiovascular risk factors, neurological and retinal health exams should be done. For example, ~40% of T2D patients have hypertension at diagnosis. Elevated pressure is a risk factor for both T2D development and complications.14

T2D increases the risk for peripheral vascular disease, stroke, and periodontal pathologies. Diabetes is also the leading cause of end-stage renal failure, visual impairment and blindness, and of non-traumatic lower limb amputations.15,16

Generalized endothelial dysfunction in diabetes can result from disparate metabolic insults that include hyperglycemia, dyslipidemia, hypertension, hyperinsulinemia, elevated levels of fatty acids, increased production of reactive oxygen species, hyperleptinemia, and cytokine-mediated inflammation.

figure 03

Treatment 

The primary goal of diabetes treatment and prevention is to normalize plasma glucose levels, which, in turn, reduces the many complications of hyperglycemia, and reduces the risk of developing T2D for those with prediabetes. To achieve these goals, improving food choices and increasing physical activity may have the greatest impact, along with targeted nutritional supplementation.

Dietary choices that consistently have the greatest benefit resemble a Mediterranean diet. They are comprised of whole foods with a low-glycemic index; they are also high in fibre, are plant-based, and are composed of mainly of fruits, vegetables, whole grains, and legumes. This type of diet has been shown to reduce glycemia in T2D patients, as well as prevent the risk of developing T2D in those with prediabetes17,18,19,20 (See Figure 3). Also, the higher the dietary fibre, the lower the fluctuations seen postprandially.

figure 04

When combined with an increase in physical activity, dietary changes have been shown to prevent diabetes more effectively than metformin, particularly among older adults (See Figure 4).

figure 05

In addition to diet and lifestyle changes, the use of PolyGlycopleX® (PGX®) is a powerful component in the prevention and treatment of T2D. Because PGX has the highest viscosity of any fibre available, and a fibre’s viscosity has been shown to be directly proportional to postprandial glycemia, PGX effectively eliminates the fluctuations in blood glucose levels following a meal seen in many diabetic patients.

PGX exerts the following benefits:

  • Reduces postprandial (after-meal) blood glucose levels;
  • Increases insulin sensitivity;
  • Reduces appetite and promotes effective weight loss;
  • Improves diabetes control;
  • Lowers blood cholesterol.

PGX typically lowers after meal blood glucose levels by approximately 35 to 70% and also lowers insulin secretion by approximately 40%, producing a whole body insulin sensitivity index improvement of nearly 60% - a phenomenal accomplishment that is unequalled by any drug or natural health product.

Other supportive therapies include:

  • Omega-3 Fatty Acids – have been shown to have significant benefit for cardiovascular disease prevention, the major cause of morbidity and mortality in diabetic patients;21
  • Broad Antioxidant Support – vitamins C&E (mixed tocopherols) have been shown to improve endothelial function, glycemic control, arterial stiffness, hypertension, oxidation status, and to reduce inflammation;22,23,24
  • Chromium – improves insulin sensitivity, and may assist with reducing central obesity and weight loss;25
  • Magnesium – in a review of nine randomized trials with T2D patients, raised HDL cholesterol and lowered fasting plasma glucose in T2D patients;26,27
  • CoQ10 – improves blood pressure, oxidative status, HbA1c, and glycemic control in diabetic patients;28
  • Botanical Support – a number of herbs have been shown to improve insulin sensitivity, reduce postprandial glucose elevations, and restore ß-cell function;29,30,31
  • Vitamin D – deficiency has been clearly associated with insulin resistance and inflammation, and the pathogenesis of both Type I and II diabetes;32
  • Alpha Lipoic Acid – has been found to reduce oxidative damage, improve glycemic control and insulin resistance, as well as symptoms of polyneuropathy.33,34,35

REFERENCES

  1. Lupi R , Del Prato S. Beta-cell apoptosis in Type II diabetes: quantitative and functional consequences. Diabetes Metab. 2008 Feb;34 Suppl 2:S56-S64.
  2. Ong KL, Cheung BM, Wong LY, Wat NM, Tan KC, Lam KS. Prevalence, treatment, and control of diagnosed diabetes in the U.S. National Health and Nutrition Examination Survey 1999-2004. Ann Epidemiol. 2008 Mar;18(3):222-229.
  3. Cowie CC, Rust KF, Ford ES, et al. Full accounting of diabetes and pre-diabetes in the U.S. population in 1988-1994 and 2005-2006. Diabetes Care. 2009 Feb;32(2):287-294.
  4. Centers for Disease Control and Prevention (CDC) . State-specific incidence of diabetes among adults – participating states, 1995-1997 and 2005-2007. MMWR Morb Mortal Wkly Rep. 2008 Oct 31;57(43):1169-1173.
  5. Snijder MB, Dekker JM, Visser M, et al. Associations of hip and thigh circumferences independent of waist circumference with the incidence of Type II diabetes: the Hoorn Study. Am J Clin Nutr. 2003 May;77(5):1192-1197.
  6. Lee CM , Huxley RR, Wildman RP, Woodward M. Indices of abdominal obesity are better discriminators of cardiovascular risk factors than BMI: a meta-analysis. J Clin Epidemiol. 2008 Jul;61(7):646-653.
  7. Sargeant LA, Khaw KT, Bingham S, et al. Fruit and vegetable intake and population glycosylated haemoglobin levels: the EPIC-Norfolk Study. Eur J Clin Nutr. 2001 May;55(5):342-348.
  8. Harding AH , Wareham NJ, Bingham SA, et al. Plasma vitamin C level, fruit and vegetable consumption, and the risk of new-onset Type II diabetes mellitus: the European prospective investigation of cancer-Norfolk prospective study. Arch Intern Med. 2008 Jul 28;168(14):1493-1499.
  9. Bazzano LA, Li TY, Joshipura KJ, Hu FB. Intake of fruit, vegetables, and fruit juices and risk of diabetes in women. Diabetes Care. 2008 Jul;31(7):1311-1317.
  10. Schulz LO , Bennett PH, Ravussin E, et al. Effects of traditional and western environments on prevalence of Type II diabetes in Pima Indians in Mexico and the U.S. Diabetes Care. 2006 Aug;29(8):1866-1871.
  11. Aroda VR, Ratner R. Approach to the patient with prediabetes. J Clin Endocrinol Metab. 2008 Sep;93(9):3259-3265.
  12. Harman-Boehm I. Continuous glucose monitoring in Type II diabetes. Diabetes Res Clin Pract. 2008 Dec 15;82 Suppl 2:S118-21.
  13. International Expert Committee. International Expert Committee report on the role of the A1C assay in the diagnosis of diabetes. Diabetes Care. 2009 Jul;32(7):1327-1334.
  14. Hypertension in Diabetes Study (HDS): I. Prevalence of hypertension in newly presenting Type II diabetic patients and the association with risk factors for cardiovascular and diabetic complications: the hypertension in diabetes study group J Hypertens. 1993 Mar;11(3):309-317.
  15. American Diabetes Association. Standards of medical care in diabetes--2008. Diabetes Care. 2008 Jan;31 Suppl 1:S12-S54.
  16. Rahman S , Rahman T, Ismail AA, Rashid AR. Diabetes-associated macrovasculopathy: pathophysiology and pathogenesis. Diabetes Obes Metab. 2007 Nov;9(6):767-780.
  17. Barnard ND, Cohen J, Jenkins DJ, et al. A low-fat vegan diet and a conventional diabetes diet in the treatment of type 2 diabetes: a randomized, controlled, 74-wk clinical trial. Am J Clin Nutr. 2009 May;89(5):1588S-1596S.
  18. Panagiotakos DB , Tzima N, Pitsavos C, et al. The association between adherence to the Mediterranean diet and fasting indices of glucose homoeostasis: the ATTICA Study. J Am Coll Nutr. 2007 Feb;26(1):32-38.
  19. Martínez-González MA, de la Fuente-Arrillaga C, Nunez-Cordoba JM, et al. Adherence to Mediterranean diet and risk of developing diabetes: prospective cohort study. BMJ. 2008 Jun 14;336(7657):1348-1351.
  20. Riccardi G, Rivellese AA, Giacco R. Role of glycemic index and glycemic load in the healthy state, in prediabetes, and in diabetes. Am J Clin Nutr. 2008 Jan;87(1):269S-274S.
  21. Wang C , Harris WS, Chung M, et al. n-3 Fatty acids from fish or fish-oil supplements, but not alpha-linolenic acid, benefit cardiovascular disease outcomes in primary-and secondary-prevention studies: a systematic review. Am J Clin Nutr. 2006 Jul;84(1):5-17.
  22. Antoniades C, Tousoulis D, Tountas C, et al. Vascular endothelium and inflammatory process, in patients with combined Type 2 diabetes mellitus and coronary atherosclerosis: the effects of vitamin C. Diabet Med. 2004 Jun;21(6):552-558.
  23. Mullan BA , Young IS, Fee H, McCance DR. Ascorbic acid reduces blood pressure and arterial stiffness in Type II diabetes. Hypertension. 2002 Dec;40(6):804-809.
  24. Jiang Q , Ames BN. Gamma-tocopherol, but not alpha-tocopherol, decreases proinflammatory eicosanoids and inflammation damage in rats. FASEB J. 2003 May;17(8):816-822.
  25. Song Y , He K, Levitan EB, Manson JE, Liu S. Effects of oral magnesium supplementation on glycaemic control in Type 2 diabetes: a meta-analysis of randomized double-blind controlled trials. Diabet Med. 2006 Oct;23(10):1050-1056.
  26. Tsuneki H , Sekizaki N, Suzuki T et al. Coenzyme Q10 prevents high glucose-induced oxidative stress in human umbilical vein endothelial cells. Eur J Pharmacol. 2007 Jul 2;566(1-3):1-10.
  27. Hodgson JM, Watts GF, Playford DA, Burke V, Croft KD. Coenzyme Q10 improves blood pressure and glycaemic control: a controlled trial in subjects with Type II diabetes. Eur J Clin Nutr. 2002 Nov;56(11):1137-1142.
  28. Watts GF, Playford DA, Croft KD, Ward NC, Mori TA, Burke V. Coenzyme Q10 improves endothelial dysfunction of the brachial artery in Type II diabetes mellitus. Diabetologia. 2002 Mar;45(3):420-426.
  29. Shanmugasundaram ER, Rajeswari G, Baskaran K, Rajesh Kumar BR, Radha Shanmugasundaram K, Kizar Ahmath B. Use of Gymnema sylvestre leaf extract in the control of blood glucose in insulin-dependent diabetes mellitus. J Ethnopharmacol. 1990 Oct;30(3):281-294.
  30. Baskaran K, Kizar Ahamath B, Radha Shanmugasundaram K, Shanmugasundaram ER. Antidiabetic effect of a leaf extract from Gymnema sylvestre in non-insulin-dependent diabetes mellitus patients. J Ethnopharmacol. 1990 Oct;30(3):295-305.
  31. Kimura T, Nakagawa K, Kubota H, et al. Food-grade mulberry powder enriched with 1-deoxynojirimycin suppresses the elevation of postprandial blood glucose in humans. J Agric Food Chem. 2007 Jul 11;55(14):5869-5874.
  32. Palomer X, González-Clemente JM, Blanco-Vaca F, Mauricio D. Role of vitamin D in the pathogenesis of Type II diabetes mellitus. Diabetes Obes Metab. 2008 Mar;10(3):185-197.
  33. Bradley R, Oberg EB, Calabrese C, Standish LJ. Algorithm for complementary and alternative medicine practice and research in Type II diabetes. J Altern Complement Med. 2007 Jan/Feb;13(1):159-176.
  34. Kamenova P. Improvement of insulin sensitivity in patients with Type II diabetes mellitus after oral administration of alpha-lipoic acid. Hormones (Athens). 2006 Oct-Dec;5(4):251-258.
  35. Tang J, Wingerchuk DM, Crum BA, et al. Alpha-lipoic acid may improve symptomatic diabetic polyneuropathy. Neurologist. 2007 May;13(3):164-167.

FIGURES

  1. LeRoith, D. ß-cell dysfunction and insulin resistance in Type II diabetes: role of metabolic and genetic abnormalities. Am J Med. 2002 Oct 28;113 Suppl 6A:5S.
  2. Harman-Boehm I. Continuous glucose monitoring in Type II diabetes. Diabetes Res Clin Pract. 2008 Dec 15;82 Suppl 2:S119.
  3. Riccardi G, Rivellese AA, Giacco R. Role of glycemic index and glycemic load in the healthy state, in prediabetes, and in diabetes. Am J Clin Nutr. 2008 Jan;87(1):271S.
  4. Knowler WC, Barrett-Connor E, Fowler SE, et al. Reduction in the incidence of Type II diabetes with lifestyle intervention or metformin. N Engl J Med. 2002 Feb 7;346(6):397.

TABLES

  1. American Diabetes Association. Standards of medical care in diabetes--2008. Diabetes Care. 2008 Jan;31 Suppl 1:S13.
Joseph Pizzorno, ND, Chairman, Scientific Advisory Board

Joseph Pizzorno, ND

Chairman, Scientific Advisory Board

Dr. Joseph E. Pizzorno, appointed by President Clinton in 2000 to the White House Commission on Complementary and Alternative Medicine Policy and by President Bush’s administration to the Medicare Coverage Advisory Committee in 2002, is one of the world’s leading authorities on science based natural medicine. A naturopathic physician, educator, researcher and expert spokesperson, he is the founding president of Bastyr University. Under his leadership, Bastyr became the first accredited, multidisciplinary university of natural medicine and the first NIH-funded center for alternative medicine research. In June 2000, Dr. Pizzorno retired after 22 years from the presidency of Bastyr University. In 1996 he was appointed to the Seattle/King County Board of Health and was a founding board member of the American Herbal Pharmacopoeia. He served as Chair of the American Public Health Association SPIG on CAM from 1999 to 2001. In 2001, he joined the Scientific Review Board of the Gateway for Cancer Research Foundation and the Institute for Functional Medicine Board of Directors (where he now serves as Chair). In 2002, he became the founding editor-in-chief of Integrative Medicine: A Clinician's Journal, the most widely distributed peer-reviewed journal in the field. In 2007, he became the Integrative Medicine and Wellness expert for WebMD. He has been a licensed naturopathic physician (with prescriptive authority) in Washington State since 1975.
 
Dr. Pizzorno has been the recipient of numerous awards and honors. In 2006 at the 50th anniversary of the founding of National College of Naturopathic Medicine, he was recognized as its most illustrious graduate. In 2004, Natural Foods Merchandiser recognized him as one of the 25 leaders in therapeutic nutrition, and he was honored by the Institute of Functional Medicine with the Linus Pauling award for his “Decades of work establishing the scientific and educational foundation of natural medicine.” In 2003, the American Holistic Medical Association recognized him as one of the 25 “Pioneers in Holistic Medicine.” In 2002, he received the “Founder’s Award for Pioneering Complementary and Alternative Medicine” by the National Foundation for Alternative Medicine. In 2001, Natural Health Magazine recognized him as one of the leading health educators in the past 30 years. In 2000, Alternative Healthcare Management recognized him as one of the four most influential leaders in alternative health care. He travels worldwide, consulting, lecturing and promoting science-based natural medicine and collaborative healthcare.
 
In 2001, Dr. Pizzorno founded SaluGenecists, Inc. to develop innovative, science based, artificial intelligence aided advice systems to provide smart, personalized health promotion and integrated care guidance for the public and practitioners. Information about the unique tools created by SaluGenecists can be found at www.salugenecists.com.
 
Dr. Pizzorno is the author of Total Wellness and co-author of the internationally acclaimed Textbook of Natural Medicine (now in its 3rd edition with over 70,000 copies bought by doctors worldwide) and its companion books Natural Medicine Instructions for Patients and the Handbook of Natural Medicine. He also co-authored the, best-selling Encyclopedia of Natural Medicine (over 1,000,000 copies in six languages), Natural Medicine for the Prevention and Treatment of Cancer and Encyclopedia of Healing Foods.

Dr. Pizzorno is Chairman, Scientific Advisory Board for Bioclinic Naturals.
 
Additional information about Dr. Pizzorno can be found at www.drpizzorno.com.

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